ResearchPad - obesity Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[Newborn body composition after maternal bariatric surgery]]> In pregnancy after Roux-en-Y gastric bypass (RYGB), there is increased risk of low birthweight in the offspring. The present study examined how offspring body composition was affected by RYGB.Material and methodsMother-newborn dyads, where the mothers had undergone RYGB were included. Main outcome measure was neonatal body composition. Neonatal body composition was assessed by dual-energy X-ray absorptiometry scanning (DXA) within 48 hours after birth. In a statistical model offspring born after RYGB were compared with a reference material of offspring and analyses were made to estimate the effect of maternal pre-pregnancy body mass index (BMI), gestational weight gain, parity, gestational age at birth and newborn sex on newborn body composition. Analyses were made to estimate the impact of maternal weight loss before pregnancy and of other effects of bariatric surgery respectively. The study was performed at a university hospital between October 2012 and December 2013.ResultsWe included 25 mother-newborn dyads where the mothers had undergone RYGB and compared them to a reference material of 311 mother-newborn dyads with comparable pre-pregnancy BMI. Offspring born by mothers after RYGB had lower birthweight (335g, p<0.001), fat-free mass (268g, p<0.001) and fat% (2.8%, p<0.001) compared with reference material. Only 2% of the average reduction in newborn fat free mass could be attributed to maternal pre-pregnancy weight loss whereas other effects of RYGB accounted for 98%. Regarding reduction in fat mass 52% was attributed to weight loss and 47% to other effects of surgery.ConclusionOffspring born after maternal bariatric surgery, had lower birthweight, fat-free mass and fat percentage when compared with a reference material. RYGB itself and not the pre-pregnancy weight loss seems to have had the greatest impact on fetal growth. ]]> <![CDATA[Health profile of adult special immigrant visa holders arriving from Iraq and Afghanistan to the United States, 2009–2017: A cross-sectional analysis]]> Between 2,000 and 19,000 Special Immigrant Visa holders (SIVH) from Iraq and Afghanistan have resettled in the United States annually since 2008.Per the Immigration and Nationality Act, SIVH, like other immigrants and refugees, must be examined by a physician before arriving in the US. Results of these overseas examinations are transmitted by the Centers for Disease Control and Prevention (CDC) to US state and local health departments via CDC’s Electronic Disease Notification system (EDN).Increasing provider knowledge about the health conditions most commonly encountered in SIVH as well as any differences in health conditions between SIVH from Iraq and Afghanistan may facilitate diagnostic screening, examination, and referrals to additional healthcare providers in the US.Information about the health of SIV populations is limited and would be beneficial for US clinicians who see SIVH in their clinics.What did the researchers do and find?In this cross-sectional analysis, we analyzed overseas medical exam data in CDC’s EDN for 19,167 SIV Iraqi and Afghan adults who resettled to the United States from April 2009 through December 2017.Among all SIVH, 56.5% were overweight or had obesity, 2.4% reported hypertension, 1.1% reported diabetes, and 19.4% reported current or previous tobacco use.In general, Iraqi SIVH were more likely to have obesity, diabetes, and be current or former smokers than Afghan SIVH.What do these findings mean?State public health agencies and clinicians screening SIVH should consider screening for diabetes among those with risk factors and prompt referral and management of obesity, hypertension, and smoking.Behavioral risk factor counseling and referral to culturally appropriate chronic disease prevention programs can be initiated at screening visits and subsequently reemphasized with primary care providers and other healthcare professionals.Limitations include the inability to obtain all SIVH records, self-reported medical history of NCDs, and underdiagnosis of NCDs such as hypertension and diabetes because formal laboratory testing for NCDs is not used during overseas medical exams. ]]> <![CDATA[Possible risk factors for poor asthma control assessed in a cross-sectional population-based study from Telemark, Norway]]> This cross-sectional study of the general population of Telemark County, Norway, aimed to identify risk factors associated with poor asthma control as defined by the Asthma Control Test (ACT), and to determine the proportions of patients with poorly controlled asthma who had undergone spirometry, used asthma medication, or been examined by a pulmonary physician. In 2014–2015, the study recruited 326 subjects aged 16–50 years who had self-reported physician-diagnosed asthma and presence of respiratory symptoms during the previous 12 months. The clinical outcome measures were body mass index (BMI), forced vital capacity (FVC) and forced expiratory volume in one second (FEV1), fractional exhaled nitric oxide (FeNO), immunoglobulin E (IgE) in serum and serum C-reactive protein (CRP). An ACT score ≤ 19 was defined as poorly controlled asthma. Overall, 113 subjects (35%) reported poor asthma control. The odds ratios (ORs) and 95% confidence intervals (CIs) for factors associated with poorly controlled asthma were: self-reported occupational exposure to vapor, gas, dust, or fumes during the previous 12 months (OR 2.0; 95% CI 1.1–3.6), body mass index ≥ 30 kg/m2 (OR 2.2; 95% CI 1.2–4.1), female sex (OR 2.6; 95% CI 1.5–4.7), current smoking (OR 2.8; 95% CI 1.5–5.3), and past smoking (OR 2.3; 95% CI 1.3–4.0). Poor asthma control was also associated with reduced FEV1 after bronchodilation (β –3.6; 95% CI –7.0 to –0.2). Moreover, 13% of the participants with poor asthma control reported no use of asthma medication, 51% had not been assessed by a pulmonary physician, and 20% had never undergone spirometry. Because these data are cross-sectional, further studies assessing possible risk factors in general and objectively measured occupational exposure in particular are needed. However, our results suggest that there is room for improvement with regards to use of spirometry and pulmonary physician referrals when a patient’s asthma is inadequately controlled.

<![CDATA[The association between national income and adult obesity prevalence: Empirical insights into temporal patterns and moderators of the association using 40 years of data across 147 countries]]> At a country level, population obesity prevalence is often associated with economic affluence, reflecting a potential adverse outcome concomitant with economic growth. We estimated the pattern and strength of the empirically observed relationship between national income and adult obesity prevalence, and the moderating role of countries’ macro-environments on this relationship.MethodsWe assembled data on national obesity prevalence, income and a range of variables that characterize macro-environments related to 147 countries from multiple international organizations and databases. We used a Bayesian hierarchical model to estimate the relationship (elasticities) between national income (using Gross Domestic Product Per Capita, GDPPC) and adult obesity prevalence, and the moderating effects of five different dimensions (globalization orientation, demographic characteristics, economic environment, labor market characteristics, and strength of health policies) of countries’ macro-environments on the income elasticities. Using the latest (2019–2024) available national income growth projections from the International Monetary Fund, we forecast future global trends in obesity prevalence.FindingsOver the 40-years 1975–2014, adult obesity prevalence increased at a declining rate with GDPPC across the 147 countries. The mean income elasticity estimates were 1.23 (95% credible interval 1.04–1.42) for males and 1.01 (0.82–1.18) for females. The elasticities were positively associated with the extent of political globalization and negatively associated with urbanization and share of agriculture in the national GDP. Income based projections indicate that obesity prevalence would continue to grow at an average annual rate of 2.47% across the studied countries during 2019–2024.ConclusionsPopulation obesity prevalence exhibits a positive relationship with national income and there is no evidence that the relationship, while weakening, actually turns negative at higher income levels (“obesity Kuznets curve”). Based on current trends, global obesity prevalence will continue to increase during 2019–2024, with the rate of growth higher in low- and middle-income countries. As most people currently live in low- and middle-income countries with rising incomes, our findings underscore the urgent societal imperatives for effective policy initiatives, especially those that target the concomitant “nutrition transition” process with economic affluence, to break or at least further weaken the positive relationship of population obesity prevalence with national income. ]]> <![CDATA[Effects of distraction on taste-related neural processing: a cross-sectional fMRI study]]> In the current obesogenic environment we often eat while electronic devices, such as smart phones, computers, or the television, distract us. Such “distracted eating” is associated with increased food intake and overweight. However, the underlying neurocognitive mechanisms of this phenomenon are unknown.ObjectiveOur aim was to elucidate these mechanisms by investigating whether distraction attenuates processing in the primary and secondary taste cortices, located in the insula and orbitofrontal cortex (OFC), respectively.MethodsForty-one healthy, normal-weight participants received fixed amounts of higher- and lower-sweetness isocaloric chocolate milk while performing a high- or low-distracting detection task during fMRI in 2 test sessions. Subsequently, we measured ad libitum food intake.ResultsAs expected, a primary taste cortex region in the right insula responded more to the sweeter drink (P < 0.001, uncorrected). Distraction did not affect this insular sweetness response across the group, but did weaken sweetness-related connectivity of this region to a secondary taste region in the right OFC (P–family-wise error, cluster, small-volume corrected = 0.020). Moreover, individual differences in distraction-related attenuation of taste activation in the insula predicted increased subsequent ad libitum food intake after distraction (= 0.36).ConclusionsThese results reveal a mechanism explaining how distraction during consumption attenuates neural taste processing. Moreover, our study shows that such distraction-induced decreases in neural taste processing contribute to individual differences in the susceptibility for overeating. Thus, being mindful about the taste of food during consumption could perhaps be part of successful prevention and treatment of overweight and obesity, which should be further tested in these target groups. This study was preregistered at the Open Science Framework as ]]> <![CDATA[Gastrointestinal Peptides as Therapeutic Targets to Mitigate Obesity and Metabolic Syndrome]]> Obesity affects over than 600 million adults worldwide resulting in multi-organ complications and major socioeconomic impact. The purpose of this review is to summarise the physiological effects as well as the therapeutic implications of the gut hormones glucagon-like peptide-1 (GLP-1), oxyntomodulin, peptide YY (PYY), and glucose-dependent insulinotropic peptide (GIP) in the treatment of obesity and type 2 diabetes.Recent FindingsClinical trials have proven that the widely used GLP-1 analogues have pleotropic effects beyond those on weight and glucose metabolism and appear to confer favourable cardiovascular and renal outcomes. However, GLP-1 analogues alone do not deliver sufficient efficacy for the treatment of obesity, being limited by their dose-dependent gastrointestinal side effects. Novel dual agonists for GLP-1/glucagon and GLP-1/GIP are being developed by the pharmaceutical industry and have demonstrated some promising results for weight loss and improvement in glycaemia over and above GLP-1 analogues. Triagonists (for example GLP-1/GIP/glucagon) are currently in pre-clinical or early clinical development.SummaryGastrointestinal hormones possess complementary effects on appetite, energy expenditure, and glucose metabolism. We highlight the idea that combinations of these hormones may represent the way forward in obesity and diabetes therapeutics. ]]> <![CDATA[Trajectories of early to mid-life adulthood BMI and incident diabetes: the China Health and Nutrition Survey]]> This longitudinal study aims to characterize distinct body mass index (BMI) trajectories during early to mid-life adulthood and to explore the association between BMI change from young adulthood to midlife and incident diabetes.Research design and methodsThis study included 7289 adults who had repeatedly measured BMI 3–9 times during 1989–2011 and information on incident diabetes. Latent class growth mixed model (LCGMM) was used to identify different BMI trajectories. Cox proportional hazard models were used to investigate the association between the trajectory group membership and incident hyperglycemia, adjusting for covariates. The hyperglycemia group included individuals with prediabetes or diabetes. The model-estimated BMI levels and slopes were calculated at each age point in 1-year intervals according to the model parameters and their first derivatives, respectively. Logistic regression analyses were used to examine the association of model-estimated levels and slopes of BMI at each age point with incident hyperglycemia. The area under the curve (AUC) was computed from longitudinal growth curve models during the follow-up for each individual. Prior to the logistic regression analyses, quartiles of total, baseline, and incremental AUC values were calculated.ResultsThree distinct trajectories were characterized by LCGMM, comprising of low-increasing group (n=5136), medium-increasing group (n=1914), and high-increasing group (n=239). Compared with the low-increasing group, adjusted HRs and 95% CIs were 1.21 (0.99 to 1.48) and 1.56 (1.06 to 2.30) for the medium-increasing and the high-increasing group, respectively. The adjusted standardized ORs of model-estimated BMI levels increased among 20–50 years, ranging from 0.98 (0.87 to 1.10) to 1.19 (1.08 to 1.32). The standardized ORs of level-adjusted linear slopes increased gradually from 1.30 (1.16 to 1.45) to 1.42 (1.21 to 1.67) during 20–29 years, then decreased from 1.41 (1.20 to 1.66) to 1.20 (1.08 to 1.33) during 30–43 years, and finally increased to 1.20 (1.04 to 1.38) until 50 years. The fourth quartile of incremental AUC (OR=1.31, 95% CI 1.03 to 1.66) was significant compared with the first quartile, after adjustment for covariates.ConclusionsThese findings indicate that the BMI trajectories during early adulthood were significantly associated with later-life diabetes. Young adulthood is a crucial period for the development of diabetes, which has implications for early prevention. ]]> <![CDATA[SAT-567 Hypertriglyceridem...From Mild to Fatal!... Is Time for Awareness]]> Hypertriglyceridemia… From mild to fatal! … Is Time for Awareness.

Hypertriglyceridemia can be primary or acquired. High triglycerides are related to complications such as pancreatitis and there is a positive correlation between hypertriglyceridemia and atherosclerotic burden. In this case series we aim to discuss pancreatitis as a hypertriglyceridemia complication and to acknowledge the importance of prevention and management. Is there something we can do to raise awareness and avoid complications as in the cases?

All cases present with chief complaint of epigastric cramp-like abdominal pain, radiating to the back, nausea/vomiting and with highly lipemic blood samples.

38y/o F admitted after been found with lipase 268 U/L (n<60 U/L), amylase 131 U/L (n<100 U/L) and findings of pancreatitis on CT scan. Patient with one-year history of T2DM refers this is the 4th episode of pancreatitis and reports that last time she was told about having triglycerides in 4,000 mg/dL for which she went to her physician that prescribe her Fenofibrate. Patient triglycerides were 7,931 mg/dL (n<199 mg/dL) and found with poorly controlled diabetes with HgbA1c 8.4%. She was properly managed, and triglycerides decrease to 1,309 mg/dL.

31y/o F with elevated lipase (237 U/L, n<60 U/L) and findings of pancreatitis on CT scan was admitted and found with 7,755 mg/dL triglycerides. She refers to have endometriosis for which she uses OCPs for >5years. She develops intractable abdominal pain along with abdominal distension and progress to Acute Respiratory Distress Syndrome (ARDS) requiring mechanical ventilation. She had a prolonged ICU stay and after management triglycerides decrease to 95mg/dL, symptoms resolve, and patient was discharge.

48y/o F with pancreatitis, lipase levels 1,452 U/L, amylase 744 U/L and positive imaging findings. Patient with uncontrolled diabetes (HgbA1c 11.0%) and breast mass s/p lumpectomy for which she used tamoxifen for the last 2 years. Triglycerides 7,444mg/dL on Gemfibrozil started due to previous levels found >4,000 mg/dL on outpatient evaluation. She deteriorates clinically and develops renal failure, abdominal compartment syndrome, respiratory distress and hypotension requiring mechanical ventilation and vasopressors. On repeated abdominal CT pancreas changes were suggestive of fulminant pancreatitis. Patient did not respond to treatment and passed away 48 hours after admission.

Hypertriglyceridemia complications can be mild or fatal as in these cases. They were evaluated by a primary care physician before complications occur and had secondary causes that predispose them to hypertriglyceridemia, but they were not addressed, reason for which these scenarios raise concern of how much we know? How much we are doing to prevent these outcomes?... Awareness of hypertriglyceridemia management and adverse effects is necessary to avoid complications and fatal outcomes. Is time!

<![CDATA[SAT-LB92 Sex Hormones Therapy Differentially Modulates HDL Function in Transgender Individuals]]> Background/aim: The main proposed atheroprotective function of high-density lipoproteins (HDL) lays on their role to promote macrophage cholesterol efflux. An insightful way to learn more about the effects of sex hormones on HDL function is to study changes during hormone therapy. The present study was aimed at evaluating the effects of exogenous sex hormones administration on HDL cholesterol efflux capacity (CEC) within transgender individuals. CEC estimates the ability of HDL to remove cholesterol from cells, i.e. the initial step in reverse cholesterol transport.

Subjects/Methods: Transmen were treated with testosterone gel, a mix of testosterone esters once every three weeks) or testosterone undecanoate once every twelve weeks, whereas transwomen were treated with either oral estradiol valerate or a transdermal application of estradiol (patches). Cyproterone acetate was prescribed as a testosterone-blocking agent to all transwomen. HDL function was evaluated by a radioisotopic technique. Hormone levels, lipids and HDL function were evaluated after one year of follow-up.

Results: In transmen (n= 15), testosterone markedly increased (+ 97%; p < 0.0001), whereas luteinizing hormone (LH) decreased significantly (- 64%; p = 0.049). Total cholesterol and low-density lipoprotein cholesterol (LDL-C) were not affected by testosterone treatment, whilst triglycerides (TG) were raised (+ 11.76%; p = 0.0078) and HDL-C reduced (- 19.6%, p=0.0103). Concerning HDL CEC, only the aqueous diffusion process was lowered (- 9.8%; p = 0.0032), an effect directly correlated with HDL-C changes (r = 0.6242, p = 0.0002). Total-, ATP-binding cassette transporter (ABCA1)-, and ABCG1-mediated CEC were not affected by testosterone treatment. In transwomen (n= 15), estradiol levels were raised (+200%, p=0.013) whereas LH and testosterone significantly reduced, i.e. - 97% for both. Relative to lipids, estradiol supplementation reduced total cholesterol (- 10.7%, p=0.0017), HDL-C (- 14.3%, p = 0.0024) and LDL-C (- 10.9%, p = 0.0058). Total HDL CEC decreased (- 11%, p=0.0001) with a specific decrement in CEC mediated by the ATP-binding cassette transporter (ABCA1) (-24%, p = 0.0003) and aqueous diffusion (-4.7%, p = 0.0014). This last was associated to a reduction in HDL-C (r = 0.4084, p = 0.0251). Conversely, the drop in ABCA1 and total CEC did not associate to reductions in HDL-C levels.

Conclusions: In transmen, testosterone supplementation was associated with a reduction in aqueous diffusion-mediated CEC, an effect potentially dependent to HDL-C changes. In transwomen, estrogen significantly decreased HDL function (CEC), independent of HDL-C levels changes.

<![CDATA[SUN-596 A Rare Presentation of Early Onset Wernicke Encephalopathy Following Sleeve Gastrectomy]]> Background: Wernicke encephalopathy (WE) has been reported after malabsorptive bariatric surgeries but is an uncommon complication of sleeve gastrectomy. Since 2011, the number of patients receiving a sleeve gastrectomy has tripled, with almost 60% of patients undergoing bariatric surgery receiving a sleeve gastrectomy in 2017 (1). We present a case of WE in a young woman as a rare and early complication of sleeve gastrectomy.

Clinical Case: A 32-year old female with a past medical history significant for hypertension, pseudotumor cerebri, and morbid obesity status post sleeve gastrectomy two months prior presented to the emergency department with complaints of blurry vision and lower extremity numbness. Physical examination showed sluggish light reflex and decreased extraocular movements. Given history of pseudotumor cerebri, patient underwent a therapeutic lumbar puncture with removal of 13 ml of CSF. Opening pressure was 20 cm of water and patient experienced no relief of her symptoms. Ophthalmology consult did not offer an explanation for the blurry vision. MRI-brain with and without contrast showed findings highly suggestive of WE. It showed faint linear symmetric hyperintensities along the bilateral mesial thalamus, dorsal midbrain and periaqueductal gray matter, which were determined to be acute in nature in comparison with a MRI performed three weeks prior. Upon further investigation, thiamine level was low at 43.6 nmol/L [66.5 – 200] confirming the diagnosis of WE. Thiamine supplementation was started immediately and patient reported improvement of her vision the next day with return to baseline in 3 days.

Conclusion: There have been a handful of cases of WE reported in literature as a complication of sleeve gastrectomy. Zheng, L also reported a case of WE 7 weeks after sleeve gastrectomy (2). Although sleeve gastrectomy does not directly affect the primary absorptive pathway of thiamine in the gastrointestinal tract, it is imperative to consider WE in patients presenting with suspicious neurologic symptoms after a recent sleeve gastrectomy. WE was suspected in our case due to typical MRI findings and neurological presentation after bariatric surgery, which was later confirmed by low serum thiamine level. Early detection and thiamine supplementation resulted in complete reversal of symptoms in our patient. WE is a rare but severe and preventable consequence of bariatric surgery that warrants attention given its rapid onset and detrimental course.

Reference: (1) Estimate of Bariatric Surgery Numbers, 2011-2017. (2018, June 26). Retrieved from (2) Zheng, L. (2016).

Wernicke Encephalopathy and Sleeve Gastrectomy. American Journal of Therapeutics, 23(6).

<![CDATA[SUN-586 CXCR2 Repression by Glucocorticoids in Adipose Tissue]]> Obesity-induced type 2 diabetes (T2D) is a significant risk factor of cardiovascular disease (CVD), which affects 28.1 million adults in the United States. Adipose tissue chronic inflammation is one of the main factors that drive obesity-induced insulin resistance (IR) and T2D. Despite several studies that have shown a link between obesity, adipose tissue inflammation, and IR/T2D, the mechanisms underlying this association are not well understood. Synthetic glucocorticoids are widely used for their potent anti-inflammatory actions; however, their use is hampered due to off-target side effects. Glucocorticoids exert profound effects on adipose tissue, including the regulation of adipocyte metabolism and immune functions. However, whether their effects on adipose tissue are positive or negative it is still a controversial topic. Genome-wide microarray data obtained from adipocyte-specific glucocorticoid receptor (GR) knockout (AdipoGRKO) mice showed that lack of GR leads to a significant increase in the expression of pro-inflammatory genes in white adipose tissue (WAT). Moreover, WAT isolated from adipoGRKO mice demonstrated significant increase in immune cell infiltration, which correlates with our gene expression data. Among the most up-regulated genes, we found the C-X-C Motif Chemokine Receptor 2 (CXCR2), which is a critical mediator of chemotaxis to the sites of inflammation. Although studies have shown the presence of CXCR2 in adipocytes and suggested the contribution of CXCR2 signaling in adipocyte development, its role in obesity-driven adipose tissue inflammation is unknown. This led us to hypothesize that adipocyte specific administration of glucocorticoids can reduce obesity-induced adipocyte inflammation by inhibiting CXCR2 gene transcription and signaling. Our in vitro studies using 3T3-L1 cells derived adipocytes showed that treatment with the synthetic glucocorticoid, Dexamethasone (Dex) led to a significant repression of CXCR2 mRNA and protein levels. Correlating with these results, Dex treatment significantly inhibited macrophage migration to adipocytes in a mechanism dependent on GR activation and repression of CXCR2. Furthermore, these results were recapitulated in vivo. Together our findings suggest that local delivery of glucocorticoids to adipose tissue could ameliorate inflammation and reduce the risk of developing IR and T2D.

<![CDATA[MON-103 Pattern and Predictors of Thyroid Dysfunction Among Paediatric Endocrine Referrals at Tertiary Care Centre: A Longitudinal Study]]> Background Post iodisation era has experienced gradual change in pattern of thyroid disorders among paediatric population with autoimmunity taking precedence over iodine deficiency disorders and subclinical hypothyroidism (SCH) now more frequently diagnosed but inappropriately managed. Aims This study was conducted to evaluate pattern of abnormal thyroid function among children referred to our tertiary care centre, to ascertain characteristics that influence treatment decisions and to follow them for various outcome measures. Design It was an observational longitudinal follow up study where all children less than 18 years, referred to our outpatient clinic for suspected thyroid disorder were recruited. Demographic data, personal and family history, clinical features were noted and laboratory tests including TT4, TT3, TSH, anti-thyroid peroxidase(antiTPO) and anti-thyroglobulin(antiTG) antibody were conducted in study subjects. Management was based on the clinical judgment of the attending endocrinologist. Patients were followed at 6 week, 3 months, 6 months and one year with clinical and laboratory work up at each visit. Results A total of 241 subjects aged 18 days to 17 years were included out of which 62.25% were females. Initial evaluation revealed SCH in 40% of refereed subjects, overt hypothyroidism (OH) in 33%, congenital hypothyroidism (CH) in 18% and overt thyrotoxicosis in 5%. Autoimmune thyroiditis constituted the major cause of hypothyroidism in the OH group with significantly higher prevalence of anti-TPO and antiTG antibody in comparison of SCH group (61% vs 31%; 45% vs 21.9%, p<0.05) respectively. All subjects in OH group were treated whereas 76% subjects in SCH group were treated and the mean dose of L thyroxine required to treat OH was significantly higher (2.31+1.1ug/kg/day vs 1.76+1.07ug/kg/day; p<0.001) in comparison of SCH group. A major independent predictor of treatment in SCH was initial TSH which was significantly higher in the treated group (11.65 + 3.80 uIU/ml vs 9.24 + 1.31 uIU/ml; p<0.001). Subjects with congenital hypothyroid presented at a mean age of 6 months (18 days to 2 years) with most common aetiology being thyroid hypoplasia and dyshormonogenesis

(20% each). Graves’ disease was diagnosed in 11 out of 12 subjects with thyrotoxicosis and were treated with antithyroid drugs. Overall 85.5% of refereed subjects were treated and after one-year follow up management was found to be adequate in 81% subjects. Conclusions The evolving trend of diagnosing children having nonspecific symptoms with SCH is a matter of concern as many are subjected to the burden of unwanted prolonged treatment and frequent testing as highlighted in our study. Delayed presentation of CH in our study warrants active surveillance of children at birth for thyroid disorders to avoid long term adverse effects on mental development.

<![CDATA[SAT-613 Comparison of CV Risk Scores to Evaluate Cardiovascular Risks in Thai Type 2 Diabetes]]> Objective: Various cardiovascular risk scores have been developed and the RAMA-EGAT risk score was developed by Thai database with minority of diabetes. This study aims to compare the predictability of the ADVANCE, UKPDS, SCORE, Framingham Risk Score (FRS) and RAMA-EGAT risk score for carotid atherosclerosis, arterial stiffness and peripheral arterial disease in Thai T2DM patients. Methods: A cross-sectional study was conducted in T2DM patients without established CVD at a tertiary care hospital. Demographic and DM-specific data were collected. Carotid intima-media thickness (CIMT), carotid plaque, cardio-ankle vascular index (CAVI) and ankle-brachial index (ABI) were measured as the markers of atherosclerosis. Risks of CVD were calculated according to the ADVANCE, UKPDS, SCORE, FRS and RAMA-EGAT risk scores. These risk scores were correlated with the atherosclerotic markers by odds ratio using logistic regression and the proper points of the risk scores to predict atherosclerosis were calculated by the areas under the curve (AUC). Results: There were 180 T2DM participants with the mean age of 60-year-old, diabetes duration of 13 years and mean A1C 7.4%. The highest sensitive risk score was FRS, following by UKPDS, SCORE, ADVANCE and RAMA-EGAT risk score, which indicated high-risk patients as 44.8%, 27.6%, 18.9%, 13.8% and 0% accordingly. There were 40.3% of the patients with arterial stiffness detected by CAVI > 9, 24.0% with carotid atherosclerosis defined by CIMT > 0.07 mm or presenting of carotid plague and 8.3% with ABI < 0.9. The odds ratios (OR) of 4 risk scores increased by the quartiles for carotid plaque, CIMT, CAVI and ABI while the OR of RAMA-EGAT scores increased by the quartiles only for carotid plaque. The highest quartile of ADVANCE, UKPDS, SCORE and FRS significantly (P<0.01) increased the risk of abnormal CIMT; OR 2.64-8.75, carotid plaque; OR 1.51-11.21, CAVI; OR 11.38-19.00, and ABI; OR 1.18-12.57. The highest quartile of RAMA-EGAT score significantly increased the risk of carotid plaque; OR 5.35 (1.44-19.91) P<0.01. ROC analysis revealed that ADVANCE > 3.0% in 4-year, UKPDS > 11% in 10-year, fatal-SCORE > 6% in 10-year and FRS > 18% in 10-year were predictive of carotid atherosclerosis with sensitivity of 76-84% and specificity of 61-69% and they were predictive of arterial stiffness with the sensitivity of 71-80% and specificity of 64-68%. Conclusion: There was no significant difference when comparing the predictability of the ADVANCE, UKPDS, FRS and SCORE risk estimation for carotid atherosclerosis, arterial stiffness and peripheral arterial disease and they were more correlative with atherosclerotic markers than RAMA-EGAT score in Thai type 2 diabetic patients.

<![CDATA[SAT-657 The Gut Microbiome Regulates Host Glucose Homeostasis via Peripheral Serotonin]]> The gut microbiome is an established regulator of aspects of host metabolism, such as glucose handling. Despite the known impacts of the gut microbiota on host glucose homeostasis, the underlying mechanisms are unknown. The gut microbiome is also a potent mediator of gut-derived serotonin synthesis, and this peripheral source of serotonin is itself a regulator of glucose homeostasis. Here, we determined whether the gut microbiome influences glucose homeostasis through effects on gut-derived serotonin. Using both pharmacological inhibition and genetic deletion of gut-derived serotonin synthesis, we find [1] that the improvements in host glucose handling caused by antibiotic-induced changes in microbiota composition are dependent on the synthesis of peripheral serotonin.

[1] The gut microbiome regulates host glucose homeostasis via peripheral serotonin. Proc Natl Acad Sci U S A. 2019 Oct 1;116(40):19802-19804. Martin AM, Yabut JM, Choo JM, Page AJ, Sun EW, Jessup CF, Wesselingh SL, Khan WI, Rogers GB, Steinberg GR, Keating DJ.

<![CDATA[SAT-573 Eruptive Xanthomas in a Patient with Hypertriglyceredemia and Type 2 Diabetes Mellitus]]> BACKGROUND: Eruptive xanthomas are rare, asymptomatic, cutaneous lesions and are markers for serious underlying metabolic disorders that demand an early diagnosis to prevent morbidity and mortality.

Clinical Case: A 27 years old obese female presented with generalized, pruritic eruptions. The eruptions had been present for approximately three weeks. Crops of firm yellow-red circumscribed Papules (diameter 1–3 mm) distributed on the extensor surfaces of both the upper and the lower extremities which were few in numbers to begin with but increased in density subsequently spreading to involve her back, abdomen, knees, and posterior thighs. The patient besides being obese had no other significant past medical or family history. Labs: FBS:258 mg/dl (80-100mg/dl), HbA1c:11.7%(<5.6%), Total lipids: 3680 mg/dl (400–1000 mg/dl), Total Cholesterol: 857 mg/dl (120–200 mg/dl), Triglycerides: 5428 mg/dl (70–150 mg/dl), HDL:15mg/dl (45–64 mg/dl), LDL: 371 mg/l(<130 mg/dl),VLDL: 402 mg/dl (<30 md/dl). Results of kidney, liver and thyroid function tests were normal, as well as amylase and lipase. X-ray chest and abdominal ultrasound were unremarkable. Biopsy of the papules was not carried out due to non-affordability on the part of the patient. The patient was managed by an interdisciplinary approach for diabetes mellitus type 2 and hyperlipidaemia. Treatment was started with oral hypoglycaemic along with lipid lowering agents and the required lifestyle modifications including weight control, adopting a low-fat diet, and regular exercise were advised. The papules resolved within six weeks of the treatment and lab reports indicated improvement in her glycemic control and hypertriglyceridemia. It was clinically diagnosed as Eruptive Xanthomas of secondary hypertriglyceridemia due to diabetes mellitus.


Recognizing eruptive xanthomas and being aware of its association with hypertriglyceridemia and diabetes mellitus can help to decrease any lag between a patient being seen by a physician and treatment for a serious medical conditions such as coronary artery disease and pancreatitis.

REFRENCES: Digby M; Belli R; McGraw T; Lee A (2011). “Eruptive xanthomas as a cutaneous manifestation of hypertriglyceridemia: a case report”. J Clin Aesthet Dermatol. 4: 44–6. PMC 3030216Freely accessible. PMID 21278899.

<![CDATA[SAT-605 Characterization of Dual Projection Patterns of Refeeding-Activated Neurons in the Parasubthalamic Nucleus]]> We have observed that following a fast, animals terminate their food intake within 2h after refeeding accompanied by a pattern of neuronal activation as identified by c-fos immunostaining that involves a number of brain regions associated with the regulation of food intake including the nucleus tractus solitarius (NTS), parabrachial nucleus (PBN), central nucleus of the amygdala (CEA), hypothalamic arcuate and paraventricular nuclei, and bed nucleus of the stria terminalis. We also observed striking c-fos activation in the posterior-lateral hypothalamus called the parasubthalamic nucleus or PSTN, raising the possibility that it may also be an important anorectic center in the brain. To establish how the PSTN is integrated into the CNS, we performed dual-label retrograde tract tracing studies to characterize whether refeeding-activated PSTN neurons project to one, or more than one target area in the CNS. Adult, Sprague-Dawley rats received dual stereotaxic injections of Alexa Fluor 488- and Alexa Fluor 555-conjugated cholera toxin β subunit (CTB; 0.1%, 0.5–1 µl volume) into the 1) PBN and NTS, 2) PBN and CEA and 3) NTS and CEA. After 7–12 days, the animals were fasted for 24 h and then given free access to food for 2 h before euthanasia by transcardial perfusion with 4% paraformaldehyde. Brains with successful dual injections were further processed for c-fos immunohistochemistry. The results showed that 26.5±3.8% of PSTN neurons projecting to the PBN also project to the CEA, and 34.6±7.6% of PSTN neurons that project to the CEA also project to the PBN. In addition, 20.2±2.7% of PSTN neurons that project to the PBN also project to the NTS, and 38.1±9.7% of PSTN neurons that project to the NTS also project to the PBN. Furthermore, 35.0±12.5% of PSTN neurons that project to the CEA project to the NTS and 37.1±4.0% of PSTN neurons that project to the NTS project to the CEA. Finally, up to 15% of the neurons with dual projections to the PBN and CEA contained c-fos after refeeding; up to 18% of the neurons with dual projections to the PBN and NTS contained c-fos; and up to 30% of neurons with dual projections to the NTS and CEA contained c-fos. We conclude that a large number of PSTN neurons have more than one projection site within the brain, thus the PSTN appears to have the capability of simultaneously communicating information about appetite to several, major feeding-related sites within the brain, presumably to terminate feeding.

<![CDATA[SAT-577 Severe Asymptomatic Hypertriglyceridemia]]> Background

Case reports of patients with severely elevated serum triglyceride levels (>1000 mg/dL) have been documented where Insulin infusions, heparin and plasmapheresis have demonstrated rapid and successful decrease in serum Triglyceride levels. The benefits of one approach versus the other to prevent major complications such as cardiovascular events or acute pancreatitis has not been well investigated. We present the case of a patient with severely elevated serum triglyceride levels without any manifestations.

Case Description

A 53-year-old male presented from his primary care provider’s office due to elevated Triglycerides levels over 6000 as per outpatient lab work. Inpatient labs were unattainable initially due to hemolysis secondary to the severely high lipid content. Patient was admitted to the medical ICU for closer monitoring and initiated on an insulin drip. Two days after insulin initiation patient’s triglyceride levels returned as 2,887 with a total cholesterol count of 848. His insulin drip was continued until his TAG levels were less than 1000. Upon discharge his levels were less than 600.


Most patients with hypertriglyceridemia are asymptomatic. However, in patients with levels above 1000 mg/dL, the risk of pancreatitis or cardiovascular event is of concern. Hypertriglyceridemia may account for 1 to 14 percent of cases of acute pancreatitis. Treatment is largely based upon symptoms and complications. In the event of pancreatitis or other cardiovascular complication, plasmapheresis is usually recommended. If asymptomatic, Insulin may be used. Insulin promotes synthesis of lipoprotein lipase which functions to hydrolyze triglycerides, and has been shown to be an effective lowering agent in the treatment of such individuals. Case reports of Heparin being used as a lipid lowering agent have also been documented, but was not used in our particular patient.

Normal triglyceride plasma levels are defined as less than 150 mg/dL. Mild hypertriglyceridemia typically ranges between 150-499 mg/dL, moderate between 500-866 mg/dL, and severe is defined as levels greater than 886 mg/dL. Plasma triglyceride levels above 1000 mg/dL occur in fewer than 1 in 5000 individuals. It is said that patients with TAG levels above 2000 mg/dL almost always have both a secondary and a genetic form of Hypertriglyceridemia. For this reason it is very important to identify these patients as early as possible to treat appropriately. Our patient was a known alcohol abuser, yet without the presence of some polygenic familial disorder, the likelihood of our patient having TAG levels >6000 mg/dL, is very unlikely.

<![CDATA[SAT-606 Distribution of Beta Klotho Gene Expression in the Mouse Brain]]> Fibroblast growth factor 21 (FGF21) has emerged as a critical endocrine factor for understanding the neurobiology of obesity, such as by the regulation thermogenesis, food preference, and metabolism, as well as for neuroprotection in Alzheimer’s disease and traumatic brain injury. FGF21 is synthesized primarily by the liver and pancreas then crosses the blood brain barrier to exert its effects in the brain. However, the sites of FGF21 action in the brain is not well-defined. FGF21 action requires the activation of FGF receptor 1c as well as its obligate co-receptor beta klotho (KLB). In order to determine the sites of FGF21 action, we mapped the distribution of Klb mRNA by in situ hybridization using RNAscope technology. We labeled Klb distribution throughout the rostrocaudal axis of male wildtype mice by amplifying Klb hybridization using tyramine signal amplification and visualizing Klb hybridization using Cyanine 3 fluorescence. The resulting Klb signal appears as punctate red “dots,” and each Klb neuron may express low (1–4 dots), medium (5–9 dots), or high levels (10+ dots) of Klb hybridization. We then mapped individual Klb expressing neuron to the atlas plates provided by the Allen Brain Atlas in order to determine Klb distribution within the substructures of each brain region, which are defined by Nissl-based parcellations of cytoarchitectural boundaries. The distribution of Klb mRNA is widespread throughout the brain, and the brain regions analyzed thus far point to notable expression in the hypothalamus, amygdala, hippocampus, and the cerebral cortex. The highest expression of Klb was localized to the suprachiasmatic nucleus in the hypothalamus, which contained low and medium Klb-expressing neurons in the lateral hypothalamic area and ventromedial hypothalamic nucleus while low expressing Klb neurons were seen in the paraventricular and dorsmedial hypothalamic nucleus. Hippocampal Klb expression was limited to the dorsal region and largely restricted to the pyramidal cell layer of the dentate gyrus, CA3, CA2, and CA1 but at low levels only. In the amygdala, low and medium Klb expressing cells were seen in lateral amygdala nucleus while low levels were observed in the basolateral amygdala nucleus. Cortical Klb expression analyzed thus far included low Klb-expressing neurons in the olfactory areas, including layers 2 and 3 of piriform cortex and nucleus of the lateral olfactory tract. These findings are consistent with the known roles of FGF21 in the central regulation of energy balance, but also implicates potentially wide-ranging effects of FGF21 such as in executive functions.

<![CDATA[SAT-LB102 Obesity Is Associated With Reduced Expression of the Anorexigenic Neuropeptide Nucleobindin-2/Nesfatin-1 in the Human Nucleus of the Solitary Tract]]> Introduction: Feeding is a complex behavior coordinated by interrelated forebrain, hypothalamic, and brainstem neuronal networks. Brainstem neurons constitute an important input for the neural circuitry integrating nutrient signals to control ingestive behavior. Orexigenic and anorexigenic neuropeptides act in concert to regulate energy balance. Data from animal models suggest that altered neuropeptidergic expression contributes to obesity. Nucleobindin-2/nesfatin-1, an appetite-suppressing neuropeptide and negative regulator of body weight, is reduced in the hypothalamus of mouse obesity models. In obese and overweight humans, we have recently reported decreased nucleobindin-2/nesfatin-1 immunoexpression in the lateral hypothalamic area, which is critically involved in appetite and metabolic regulation and has extensive connections with brainstem feeding circuits. Objective: The present study explored nucleobindin-2/nesfatin-1 localization pattern as well as the association between nucleobindin-2/nesfatin-1 protein expression and body weight in human brainstem nuclei. Methods: Sections of 20 human brainstems (13 males, 7 females; 8 normal weight, 6 overweight, 6 obese) were examined by means of immunohistochemistry and double immunofluorescence labeling. Results: Nucleobindin-2/nesfatin-1 widespread distribution was observed in various brainstem areas, including nuclei with well-defined roles in energy homeostasis and in autonomic and behavioral processes, such as the nucleus of the solitary tract, dorsal motor nucleus of vagus, area postrema, inferior olive, raphe nuclei, reticular formation, locus coeruleus, parabrachial nuclei, and pontine nuclei, and in Purkinje cells of the cerebellum. Interestingly, nucleobindin-2/nesfatin-1 immunofluorescence signal extensively localized in neuronal subpopulations expressing neuropeptide Y and cocaine- and amphetamine-regulated transcript (peptides known to exert potent actions on food intake and energy balance) in nucleus of the solitary tract, inferior olive, locus coeruleus, and dorsal raphe nucleus. Of note, nucleobindin-2/nesfatin-1 immunoexpression was significantly lower in obese than normal weight subjects in the nucleus of the solitary tract (p<0.05). Conclusions: These data provide for the first time neuroanatomical support for the potential role of nucleobindin-2/nesfatin-1 in human brainstem circuits controlling energy homeostasis. In nucleus of the solitary tract, a key integrator of nutrient state signals and a neural substrate of food reward-related processes, altered neurochemistry such as nucleobindin-2/nesfatin-1 deficiency may contribute to dysregulation of homeostatic and/or hedonic feeding behavior and ultimately to obesity.

<![CDATA[MON-LB108 Measurement Of Carotid Intima,hepatic Steatosis And Inflammatory Markers In Obese Children]]> Measurement of carotid intima,hepatic steatosis and inflammatory markers in obese children. Elevated levels of inflammatory factors and increased mean intimal carotid thickness (IMT) would increase the risk of atherothrombotic events and contribute to the progression of cardiovascular disease in obese children. Objectives: Evaluate inflammatory factors, metabolic syndrome and non-alcoholic liver steatosis and carotid IMT as an early cardiovascular risk marker. Patients and methods: Descriptive cross-sectional exploratory study. Consider 41 obese children both sexes between 6- 12 years old. Evaluated: anthropometry and determinations of lipid and liver profile, blood glucose, insulin, HOMA, ultrasensitive CRP, fibrinogen. Hepatic ultrasound and measurement of carotid IMT with ESAOTE Mylab 50 Exdicion equipment. . Results: From 41 studied patients, 57% were female. 51% presented MS and 68% elevated triglycerides. CRP> 1 was found in 71% of cases. Hepatic steatosis was observed in 60%, which only 10% had altered transaminases. 12% presented high fibrinogen. Patients with MS had a significant positive difference in the IMTCC (X = 0.41 ± 0.12; p 0.024), HDL (X 37.89 ± 1.72; p 0.004) triglycerides (X 149.42 ± 10.69; p 0.002) in relation to patients without MS. Conclusion: CRP is an inflammatory risk factor associated with elevated BMI and MS. There was a higher prevalence of MS in our study. The increase in the average intimal thickness is significantly related to the presence of MS and RCP>1. The determination of marker molecules of an inflammatory state and measurement of carotid IMT would contribute to the implementation of strategies to prevent cardiovascular, hepatic and metabolic risk since childhood.