ResearchPad - diet-and-type-2-diabetes https://www.researchpad.co Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[Brazilian vegetarians diet quality markers and comparison with the general population: A nationwide cross-sectional study]]> https://www.researchpad.co/article/elastic_article_7851 Vegetarianism is an increasingly common practice worldwide. Despite good evidence from other countries regarding vegetarians’ diet quality, data from the Brazilian population is still scarce.ObjectiveTo characterize the vegetarian Brazilian population and evaluate their diet quality compared to the general Brazilian population.MethodsWe performed a nationwide cross-sectional study using an online self-administered questionnaire, previously validated for the Brazilian population, to evaluate diet quality markers of vegetarians. The invitation to participate in the survey was spread nationwide, aimed at vegetarian communities. Individuals who considered themselves vegetarians and were at least 18 years old were eligible to participate. The results on regular intake and intake adequacy were compared among vegetarians and between genders using the Pearson’s chi-square test. The body mass index (BMI) were analyzed by the Analysis of Variance (ANOVA) followed by Tukey post-hoc test. The Kolmogorov-Smirnov test verified normality. All analyses considered bilateral hypotheses and a significance level of 5% (p <0.05).ResultsBrazilian vegetarians presented better diet quality markers, such as higher regular weekly intake and adequate daily intake of fruits and vegetables, and lower regular intake of soft drinks when compared to the general Brazilian population. Vegetarians also presented a proportionally higher consumption of natural foods and lower consumption of processed foods. Among vegetarians, a higher proportion of vegans showed positive results regarding diet markers analysis, when compared to vegetarians, pesco-vegetarians, and semi-vegetarians.ConclusionsVegetarians showed better results of diet adequacy when compared to the general population in Brazil, and vegans fared better when compared with other vegetarians. Despite the good results found, a large proportion of the participants still did not achieve the fruits and vegetables daily intake, according to the World Health Organization recommendations. ]]> <![CDATA[The self-care dilemma of type 2 diabetic patients: The mechanism of self-regulation resource depletion]]> https://www.researchpad.co/article/5c12cf95d5eed0c4849149d3

Self-care is important for type 2 diabetes mellitus (T2DM) patients’ disease prognosis, but there is a common phenomenon of self-regulation failure in T2DMs. In order to figure this problem out, the current study explored the interaction between self-regulation resource depletion and diabetes self-care based on the limited resource model of self-regulation. 104 patients were surveyed using the Self-Regulatory Fatigue Scale (SRF-S) and the Diabetes Self-care Scale (DSCS) in study 1. Study 2 recruited 30 T2DM patients and 30 healthy controls, and used a sequential-task paradigm to test the effect of self-regulation resource depletion on them. Participants in study 3 were 60 T2DM patients under different levels of self-regulation resource depletion manipulation, and their self-regulation performance was recorded and compared. Study 1 indicated that the correlation between self-regulation resource depletion and exercise and diet was significant and negative, suggesting that patients with greater self-regulation resource depletion performed poorly in exercise and diet. In Study 2, T2DM patients exhibited a poorer performance on the Spatial Incompatibility Task than the participants in the control group, suggesting that their self-regulation resource was insufficient. Study 3 indicated that there was no difference in Spatial Incompatibility Task performance, reaction time or error number among patients who were requested to complete a dietary record for one week and patients who were only requested to record eating times. This research demonstrated that low levels of diabetes self-care execution was associated with patients’ deficiency in self-regulatory resource, and self-care as a series of goal-directed behaviors consumed patients’ self-regulatory resources before these behaviors became a habit.

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<![CDATA[At similar weight loss, dietary composition determines the degree of glycemic improvement in diet-induced obese C57BL/6 mice]]> https://www.researchpad.co/article/5b603630463d7e4090b7ce1f

Background

Achieving weight loss is the cornerstone of the treatment of the metabolic consequences of obesity, in particular of glucose intolerance.

Objective

To determine whether improvement in glucose control depends on dietary macronutrient composition of the diet at identical weight loss.

Materials and methods

Twenty-two weeks old diet-induced obese C57BL/6 mice lost weight through caloric restriction on normal chow (R-NC) or high fat diet (R-HF). Control mice were fed normal chow (LEAN) or high fat diet (OBESE) ad libitum. Body weight and composition were assessed after 8 weeks of dietary intervention. Glucose homeostasis was evaluated by intraperitoneal glucose tolerance tests (IPGTT). Epididymal white adipose (eWAT) and hepatic tissues were analyzed by immunohistochemistry and RT-qPCR.

Results

By 30 weeks of age, the body weight of the mice on R-NC (31.6±1.7g, mean±SEM) and R-HF (32.3±0.9g) was similar to LEAN mice (31.9±1.4g), while OBESE mice weighed 51.7±2.4g. Glucose tolerance in R-NC was better than in LEAN mice (69% AUC IPGTT, P 0.0168) whereas R-HF mice remained significantly less glucose tolerant (125% AUC IPGTT, P 0.0279 vs LEAN), despite identical weight loss. The eWAT pads and adipocyte size were similar in LEAN and R-NC mice, while the eWAT pad size of R-HF was 180% of R-NC (P < 0.0001) and the average adipocyte size of R-HF mice was 134% of R-NC fed mice (P 0.0285). No LEAN or R-NC mice had hepatic steatosis, in contrast to 28.6% of R-HF mice. Compared to OBESE mice, inflammatory markers were lower in eWAT and liver tissue of R-NC, but not in R-HF mice. Measures of visceral adiposity correlated well with glucose tolerance parameters.

Conclusions

In mice, caloric restriction on a normal chow diet improved glucose tolerance significantly more when identical weight loss was achieved on a high fat diet.

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<![CDATA[Low-Dose Aspartame Consumption Differentially Affects Gut Microbiota-Host Metabolic Interactions in the Diet-Induced Obese Rat]]> https://www.researchpad.co/article/5989daa1ab0ee8fa60ba604f

Aspartame consumption is implicated in the development of obesity and metabolic disease despite the intention of limiting caloric intake. The mechanisms responsible for this association remain unclear, but may involve circulating metabolites and the gut microbiota. Aims were to examine the impact of chronic low-dose aspartame consumption on anthropometric, metabolic and microbial parameters in a diet-induced obese model. Male Sprague-Dawley rats were randomized into a standard chow diet (CH, 12% kcal fat) or high fat (HF, 60% kcal fat) and further into ad libitum water control (W) or low-dose aspartame (A, 5–7 mg/kg/d in drinking water) treatments for 8 week (n = 10–12 animals/treatment). Animals on aspartame consumed fewer calories, gained less weight and had a more favorable body composition when challenged with HF compared to animals consuming water. Despite this, aspartame elevated fasting glucose levels and an insulin tolerance test showed aspartame to impair insulin-stimulated glucose disposal in both CH and HF, independently of body composition. Fecal analysis of gut bacterial composition showed aspartame to increase total bacteria, the abundance of Enterobacteriaceae and Clostridium leptum. An interaction between HF and aspartame was also observed for Roseburia ssp wherein HF-A was higher than HF-W (P<0.05). Within HF, aspartame attenuated the typical HF-induced increase in the Firmicutes:Bacteroidetes ratio. Serum metabolomics analysis revealed aspartame to be rapidly metabolized and to be associated with elevations in the short chain fatty acid propionate, a bacterial end product and highly gluconeogenic substrate, potentially explaining its negative affects on insulin tolerance. How aspartame influences gut microbial composition and the implications of these changes on the development of metabolic disease require further investigation.

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<![CDATA[Prenatal Metformin Exposure in a Maternal High Fat Diet Mouse Model Alters the Transcriptome and Modifies the Metabolic Responses of the Offspring]]> https://www.researchpad.co/article/5989daf4ab0ee8fa60bc23d4

Aims

Despite the wide use of metformin in metabolically challenged pregnancies, the long-term effects on the metabolism of the offspring are not known. We studied the long-term effects of prenatal metformin exposure during metabolically challenged pregnancy in mice.

Materials and Methods

Female mice were on a high fat diet (HFD) prior to and during the gestation. Metformin was administered during gestation from E0.5 to E17.5. Male and female offspring were weaned to a regular diet (RD) and subjected to HFD at adulthood (10-11 weeks). Body weight and several metabolic parameters (e.g. body composition and glucose tolerance) were measured during the study. Microarray and subsequent pathway analyses on the liver and subcutaneous adipose tissue of the male offspring were performed at postnatal day 4 in a separate experiment.

Results

Prenatal metformin exposure changed the offspring's response to HFD. Metformin exposed offspring gained less body weight and adipose tissue during the HFD phase. Additionally, prenatal metformin exposure prevented HFD-induced impairment in glucose tolerance. Microarray and annotation analyses revealed metformin-induced changes in several metabolic pathways from which electron transport chain (ETC) was prominently affected both in the neonatal liver and adipose tissue.

Conclusion

This study shows the beneficial effects of prenatal metformin exposure on the offspring's glucose tolerance and fat mass accumulation during HFD. The transcriptome data obtained at neonatal age indicates major effects on the genes involved in mitochondrial ATP production and adipocyte differentiation suggesting the mechanistic routes to improved metabolic phenotype at adulthood.

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<![CDATA[Factors that Affect Pancreatic Islet Cell Autophagy in Adult Rats: Evaluation of a Calorie-Restricted Diet and a High-Fat Diet]]> https://www.researchpad.co/article/5989da37ab0ee8fa60b86879

Aging may be a risk factor for type 2 diabetes in the elderly. Dietary intervention can affect glucose tolerance in adults, which may be due to body composition and islet cell autophagy. The aim of this study was to determine the effects of various dietary interventions on islet cell autophagy. Pancreatic tissue and blood samples were collected from Sprague Dawley rats (14–16 months old, n = 15 for each group) that received a normal diet (ND), a high-fat diet (HFD), or a calorie-restricted diet (CRD). The body weight (BW), visceral fat, serum lipid levels, fasting serum glucose, insulin levels, and β/α cell area were determined in 14-16-(0-w), 16-18-(8-w), and 18-20(16-w)-month-old rats. Pancreatic islet autophagy (LC3B and LAMP2), AP (Acid Phosphatase) and apoptosis (apoptosis index, AI (TUNEL assay) and cleaved caspase-3) were detected using immunohistochemistry, ELISA and western blot. At 16 weeks, the expressions of LC3B, LAMP2 and AP markedly increased in both the HFD (P<0.01) and CRD (P<0.05) groups; however, an increase in the AI (P<0.05), cleaved caspase-3 and Beclin1 expression and a decrease in the expressions of BCL2 and BCLXL (P<0.05) were observed in only the HFD group. FFA, triglyceride levels, HOMA-IR, insulin levels and glucagon levels were significantly increased in the HFD group but decreased in the CRD group at 16 weeks (P<0.05). The degree of islet cell autophagy was potentially regulated by the levels of FFA and islet cell insulin and glucagon, which may have been due to the effects of Beclin1/BCL2.

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<![CDATA[Stress increases the risk of type 2 diabetes onset in women: A 12-year longitudinal study using causal modelling]]> https://www.researchpad.co/article/5989db4fab0ee8fa60bdba43

Background

Type 2 diabetes is associated with significant morbidity and mortality. Modifiable risk factors have been found to contribute up to 60% of type 2 diabetes risk. However, type 2 diabetes continues to rise despite implementation of interventions based on traditional risk factors. There is a clear need to identify additional risk factors for chronic disease prevention. The aim of this study was to examine the relationship between perceived stress and type 2 diabetes onset, and partition the estimates into direct and indirect effects.

Methods and findings

Women born in 1946–1951 (n = 12,844) completed surveys for the Australian Longitudinal Study on Women’s Health in 1998, 2001, 2004, 2007 and 2010. The total causal effect was estimated using logistic regression and marginal structural modelling. Controlled direct effects were estimated through conditioning in the regression model. A graded association was found between perceived stress and all mediators in the multivariate time lag analyses. A significant association was found between hypertension, as well as physical activity and body mass index, and diabetes, but not smoking or diet quality. Moderate/high stress levels were associated with a 2.3-fold increase in the odds of diabetes three years later, for the total estimated effect. Results were only slightly attenuated when the direct and indirect effects of perceived stress on diabetes were partitioned, with the mediators only explaining 10–20% of the excess variation in diabetes.

Conclusions

Perceived stress is a strong risk factor for type 2 diabetes. The majority of the effect estimate of stress on diabetes risk is not mediated by the traditional risk factors of hypertension, physical activity, smoking, diet quality, and body mass index. This gives a new pathway for diabetes prevention trials and clinical practice.

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<![CDATA[Higher body mass index and lower intake of dairy products predict poor glycaemic control among Type 2 Diabetes patients in Malaysia]]> https://www.researchpad.co/article/5989db4fab0ee8fa60bdbb51

This cross-sectional study was designed to determine factors contributing to glyceamic control in order to provide better understanding of diabetes management among Type 2 Diabetes patients. A pre-tested structured questionnaire was used to obtain information on socio-demographic and medical history. As a proxy measure for glycaemic control, glycosylated haemoglobin (HbA1c) was obtained as secondary data from the medical reports. Perceived self-care barrier on diabetes management, diet knowledge and skills, and diet quality were assessed using pretested instruments. With a response rate of 80.3%, 155 subjects were recruited for the study. Mean HbA1c level of the subjects was 9.02 ± 2.25% with more than 70% not able to achieve acceptable level in accordance to WHO recommendation. Diet quality of the subjects was unsatisfactory especially for vegetables, fruits, fish and legumes as well as from the milk and dairy products group. Higher body mass index (BMI), poorer medication compliance, lower diet knowledge and skill scores and lower intake of milk and dairy products contributed significantly on poor glycaemic control. In conclusion, while perceived self-care barriers and diet quality failed to predict HbA1c, good knowledge and skill ability, together with appropriate BMI and adequate intake of dairy products should be emphasized to optimize glycaemic control among type 2 diabetes patients.

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<![CDATA[Appropriate Insulin Level in Selecting Fortified Diet-Fed, Streptozotocin-Treated Rat Model of Type 2 Diabetes for Anti-Diabetic Studies]]> https://www.researchpad.co/article/5989db52ab0ee8fa60bdc8b9

Background

Pathophysiological investigation of disease in a suitable animal model is a classical approach towards development of a credible therapeutic strategy. This study examined appropriate insulin level in selecting animal model for type 2 diabetes (T2D) studies.

Method

Albino Wistar rats (150-200g) were divided into two groups fed with commercially available normal-diet-feed (NDF) and water or fortified diet feed (FDF) (10g NDF per gram of margarine) with 20% fructose solution as drinking water. After 6 weeks of dietary regimen both groups were divided into 5 sub-groups and injected intraperitoneally with a graded dose of streptozotocin (STZ) (0, 25, 35, 45 & 55mg/kg bw.).

Result

The result showed that the FDF-fed rats increased significantly in body weight, basal serum insulin, total cholesterol, triglycerides and blood glucose levels as compared to NDF-fed rats. Ten days post STZ induction, the groups treated with STZ (45 & 55 mg/kg) developed frank hyperglycaemia with < 46.8% serum insulin, a severe deficiency typical of diabetes type 1. The NDF25 and NDF35 groups with 75.7% and 64.4% serum insulin respectively presented relative normoglycemia, whereas the FDF35 (85.8% serum insulin) were notably hyperglycaemia (>300 mg/dL) throughout the 6weeks post diabetes confirmation. These FDF35 rats were sensitive to glibenclamide, metformin and pioglitazone in lowering hyperglycaemia, hypertriglyceridemia and hypercholesterolemia

Conclusion

The hyperglycaemia stability of the FDF35 rats (85.5% insulin) together with their sensitivity to 3 different hypoglycaemic drugs strongly suggests their suitability as a non-genetic model of T2D. Hence the study shows that circulating serum insulin ≥ 85.8% with overt hyperglycaemia may be utilized as the benchmark in selecting rat models for T2D studies.

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<![CDATA[Clustering of four major lifestyle risk factors among Korean adults with metabolic syndrome]]> https://www.researchpad.co/article/5989db50ab0ee8fa60bdc17d

The purpose of this study was to investigate the clustering pattern of four major lifestyle risk factors—smoking, heavy drinking, poor diet, and physical inactivity—among people with metabolic syndrome in South Korea. There were 2,469 adults with metabolic syndrome aged 30 years or older available with the 5th Korean National Health and Nutrition Examination Survey dataset. We calculated the ratio of the observed to expected (O/E) prevalence for the 16 different combinations and the prevalence odds ratios (POR) of four lifestyle risk factors. The four lifestyle risk factors tended to cluster in specific multiple combinations. Smoking and heavy drinking was clustered (POR: 1.86 for male, 4.46 for female), heavy drinking and poor diet were clustered (POR: 1.38 for male, 1.74 for female), and smoking and physical inactivity were also clustered (POR: 1.48 for male). Those who were male, younger, low-educated and living alone were much more likely to have a higher number of lifestyle risk factors. Some helpful implications can be drawn from the knowledge on clustering pattern of lifestyle risk factors for more effective intervention program targeting metabolic syndrome.

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<![CDATA[Opportunities and Challenges in Developing a Cohort of Patients with Type 2 Diabetes Mellitus Using Electronic Primary Care Data]]> https://www.researchpad.co/article/5989db28ab0ee8fa60bd0c44

Purpose

To develop a cohort of patients with T2DM treated with insulin using CPRD to obtain an accurate diagnosis date. This was used to analyse time from T2DM diagnosis to first ever insulin prescription between 01/01/2000 and 30/06/2012, for patients in England and Wales.

Methods

Patients aged 18 years and over at diagnosis, were included if prescribed an anti-diabetic drug and were excluded if first diagnosis-specific code was inconsistent with a T2DM diagnosis. Diagnosis codes were split into 8 categories based on whether they related to specific T2DM or non-specific diabetes codes. Patients were excluded if they had non-specific diagnosis codes and were prescribed insulin as their first-ever treatment for diabetes. Descriptive statistics for time from T2DM diagnosis to insulin initiation were calculated.

Results

Two hundred and fifty-six codes were identified which were consistent with a first-ever diagnosis of T2DM. 7 codes were considered to clearly define a diagnosis of T2DM, which were reported for 64% of patients. The final cohort comprised 11,917 patients and the median time to first insulin prescription from the date of diagnosis was 4.4 years.

Conclusions

A clear definition of cohort development is required to compare and interpret results from studies. Use of diagnosis and product codes is essential when examining use of drugs such as insulin, where competing diagnoses need to be considered separately.

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<![CDATA[Intestine-Targeted DGAT1 Inhibition Improves Obesity and Insulin Resistance without Skin Aberrations in Mice]]> https://www.researchpad.co/article/5989daceab0ee8fa60bb51f9

Objective

Diacylglycerol O-acyltransferase 1 (DGAT1) catalyzes the final committed step in triglyceride biosynthesis. DGAT1 null mice are known to be resistant to diet-induced obesity, and more insulin sensitive relative to the wild-type; however, the mice exhibit abnormalities in the skin. This work determined whether the intestine-targeted DGAT1 inhibitor could improve obesity and insulin resistance without skin aberrations in mice.

Design and Methods

We synthesized 2 DGAT1 inhibitors: Compound A, described in the patent application from the Japan Tobacco, and Compound B (A-922500), reported by Abbott Laboratories. Both compounds were evaluated for inhibitory activities against DGAT1 enzymes and effects on the skin in mice in vivo. Compound B was further investigated for effects on obesity and insulin resistance in diet-induced-obese (DIO) mice.

Results

The 2 compounds comparably inhibited the DGAT1 enzyme activity and the cellular triglyceride synthesis in vitro, while they showed different distribution patterns in mice in vivo. Compound A, which distributed systemically, caused skin aberrations, while Compound B, which preferentially distributed to the intestine, improved obesity and insulin resistance without skin aberrations in DIO mice.

Conclusions

Our results suggest that the intestine is the key tissue in which DGAT1 plays a role in promoting obesity and insulin resistance.

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<![CDATA[A four-day Western-style dietary intervention causes reductions in hippocampal-dependent learning and memory and interoceptive sensitivity]]> https://www.researchpad.co/article/5989db4fab0ee8fa60bdbb25

In animals, a Western style diet–high in saturated fat and added sugar–causes impairments in hippocampal-dependent learning and memory (HDLM) and perception of internal bodily state (interoception). In humans, while there is correlational support for a link between Western-style diet, HDLM, and interoception, there is as yet no causal data. Here, healthy individuals were randomly assigned to consume either a breakfast high in saturated fat and added sugar (Experimental condition) or a healthier breakfast (Control condition), over four consecutive days. Tests of HDLM, interoception and biological measures were administered before and after breakfast on the days one and four, and participants completed food diaries before and during the study. At the end of the study, the Experimental condition showed significant reductions in HDLM and reduced interoceptive sensitivity to hunger and fullness, relative to the Control condition. The Experimental condition also showed a markedly different blood glucose and triglyceride responses to their breakfast, relative to Controls, with larger changes in blood glucose across breakfast being associated with greater reductions in HDLM. The Experimental condition compensated for their energy-dense breakfast by reducing carbohydrate intake, while saturated fat intake remained consistently higher than Controls. This is the first experimental study in humans to demonstrate that a Western-style diet impacts HDLM following a relatively short exposure–just as in animals. The link between diet-induced HDLM changes and blood glucose suggests one pathway by which diet impacts HDLM in humans.

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<![CDATA[The Eatwell Guide: Modelling the Health Implications of Incorporating New Sugar and Fibre Guidelines]]> https://www.researchpad.co/article/5989dae5ab0ee8fa60bbd219

Objective

To model population health impacts of dietary changes associated with the redevelopment of the UK food-based dietary guidelines (the ‘Eatwell Guide’).

Method

Using multi-state lifetable methods, we modelled the impact of dietary changes on cardiovascular disease, diabetes and cancers over the lifetime of the current UK population. From this model, we determined change in life expectancy and disability-adjusted life years (DALYs) that could be averted.

Results

Changing the average diet to that recommended in the new Eatwell Guide, without increasing total energy intake, could increase average life expectancy by 5.4 months (95% uncertainty interval: 4.7 to 6.2) for men and 4.0 months (3.4 to 4.6) for women; and avert 17.9 million (17.6 to 18.2) DALYs over the lifetime of the current population. A large proportion of the health benefits are from prevention of type 2 diabetes, with 440,000 (400,000 to 480,000) new cases prevented in men and 340,000 (310,000 to 370,000) new cases prevented in women, over the next ten years. Prevention of cardiovascular diseases and colorectal cancer is also large. However, if the diet recommended in the new Eatwell Guide is achieved with an accompanying increase in energy intake (and thus an increase in body mass index), around half the potential improvements in population health will not be realised.

Conclusions

The dietary changes required to meet recommendations in the Eatwell Guide, which include eating more fruits and vegetables and less red and processed meats and dairy products, are large. However, the potential population health benefits are substantial.

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<![CDATA[The effect of meal frequency in a reduced-energy regimen on the gastrointestinal and appetite hormones in patients with type 2 diabetes: A randomised crossover study]]> https://www.researchpad.co/article/5989db50ab0ee8fa60bdc132

Background

Appetite and gastrointestinal hormones (GIHs) participate in energy homeostasis, feeding behavior and regulation of body weight. We demonstrated previously the superior effect of a hypocaloric diet regimen with lower meal frequency (B2) on body weight, hepatic fat content, insulin sensitivity and feelings of hunger compared to the same diet divided into six smaller meals a day (A6). Studies with isoenergetic diet regimens indicate that lower meal frequency should also have an effect on fasting and postprandial responses of GIHs. The aim of this secondary analysis was to explore the effect of two hypocaloric diet regimens on fasting levels of appetite and GIHs and on their postprandial responses after a standard meal. It was hypothesized that lower meal frequency in a reduced-energy regimen leading to greater body weight reduction and reduced hunger would be associated with decreased plasma concentrations of GIHs: gastric inhibitory peptide (GIP), glucagon-like peptide-1(GLP-1), peptide YY(PYY), pancreatic polypeptide (PP) and leptin and increased plasma concentration of ghrelin. The postprandial response of satiety hormones (GLP-1, PYY and PP) and postprandial suppression of ghrelin will be improved.

Methods

In a randomized crossover study, 54 patients suffering from type 2 diabetes (T2D) underwent both regimens. The concentrations of GLP-1, GIP, PP, PYY, amylin, leptin and ghrelin were determined using multiplex immunoanalyses.

Results

Fasting leptin and GIP decreased in response to both regimens with no difference between the treatments (p = 0.37 and p = 0.83, respectively). Fasting ghrelin decreased in A6 and increased in B2 (with difference between regimens p = 0.023). Fasting PP increased in B2with no significant difference between regimens (p = 0.17). Neither GLP-1 nor PYY did change in either regimen. The decrease in body weight correlated negatively with changes in fasting ghrelin (r = -0.4, p<0.043) and the postprandial reduction of ghrelin correlated positively with its fasting level (r = 0.9, p<0.001). The postprandial responses of GIHs and appetite hormones were similar after both diet regimens.

Conclusions

Both hypocaloric diet regimens reduced fasting leptin and GIP and postprandial response of GIP comparably. The postprandial responses of GIHs and appetite hormones were similar after both diet regimens. Eating only breakfast and lunch increased fasting plasma ghrelin more than the same caloric restriction split into six meals. The changes in fasting ghrelin correlated negatively with the decrease in body weight. These results suggest that for type 2 diabetic patients on a hypocaloric diet, eating larger breakfast and lunch may be more efficient than six smaller meals during the day.

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<![CDATA[Resveratrol Ameliorates High Glucose and High-Fat/Sucrose Diet-Induced Vascular Hyperpermeability Involving Cav-1/eNOS Regulation]]> https://www.researchpad.co/article/5989db0bab0ee8fa60bca2d2

Vascular endothelial hyperpermeability is one of the manifestations of endothelial dysfunction. Resveratrol (Res) is considered to be beneficial in protecting endothelial function. However, currently, the exact protective effect and involved mechanisms of Res on endothelial dysfunction-hyperpermeability have not been completely clarified. The aim of present study is to investigate the effects of Res on amelioration of endothelial hyperpermeability and the role of caveolin-1 (Cav-1)/endothelial nitric oxide synthase (eNOS) pathway. Adult male Wistar rats were treated with a normal or high-fat/sucrose diet (HFS) with or without Res for 13 weeks. HFS and in vitro treatment with high glucose increased hyperpermeability in rat aorta, heart, liver and kidney and cultured bovine aortic endothelial cells (BAECs), respectively, which was attenuated by Res treatment. Application of Res reversed the changes in eNOS and Cav-1 expressions in aorta and heart of rats fed HFS and in BAECs incubated with high glucose. Res stimulated the formation of NO inhibited by high glucose in BAECs. Beta-Cyclodextrin (β-CD), caveolae inhibitor, showed the better beneficial effect than Res alone to up-regulate eNOS phosphorylative levels, while NG-Nitro-77 L-arginine methyl ester (L-NAME), eNOS inhibitor, had no effect on Cav-1 expression. Our studies suggested that HFS and in vitro treatment with high glucose caused endothelial hyperpermeability, which were ameliorated by Res at least involving Cav-1/eNOS regulation.

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<![CDATA[Effects of Incretin-Based Therapies on Neuro-Cardiovascular Dynamic Changes Induced by High Fat Diet in Rats]]> https://www.researchpad.co/article/5989da6bab0ee8fa60b92e26

Background and Aims

Obesity promotes cardiac and cerebral microcirculatory dysfunction that could be improved by incretin-based therapies. However, the effects of this class of compounds on neuro-cardiovascular system damage induced by high fat diet remain unclear. The aim of this study was to investigate the effects of incretin-based therapies on neuro-cardiovascular dysfunction induced by high fat diet in Wistar rats.

Methods and Results

We have evaluated fasting glucose levels and insulin resistance, heart rate variability quantified on time and frequency domains, cerebral microcirculation by intravital microscopy, mean arterial blood pressure, ventricular function and mitochondrial swelling. High fat diet worsened biometric and metabolic parameters and promoted deleterious effects on autonomic, myocardial and haemodynamic parameters, decreased capillary diameters and increased functional capillary density in the brain. Biometric and metabolic parameters were better improved by glucagon like peptide-1 (GLP-1) compared with dipeptdyl peptidase-4 (DPP-4) inhibitor. On the other hand, both GLP-1 agonist and DPP-4 inhibitor reversed the deleterious effects of high fat diet on autonomic, myocardial, haemodynamic and cerebral microvascular parameters. GLP-1 agonist and DPP-4 inhibitor therapy also increased mitochondrial permeability transition pore resistance in brain and heart tissues of rats subjected to high fat diet.

Conclusion

Incretin-based therapies improve deleterious cardiovascular effects induced by high fat diet and may have important contributions on the interplay between neuro-cardiovascular dynamic controls through mitochondrial dysfunction associated to metabolic disorders.

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<![CDATA[The Flavones Apigenin and Luteolin Induce FOXO1 Translocation but Inhibit Gluconeogenic and Lipogenic Gene Expression in Human Cells]]> https://www.researchpad.co/article/5989db44ab0ee8fa60bd7f28

The flavones apigenin (4′,5,7,-trihydroxyflavone) and luteolin (3′,4′,5,7,-tetrahydroxyflavone) are plant secondary metabolites with antioxidant, antiinflammatory, and anticancer activities. We evaluated their impact on cell signaling pathways related to insulin-resistance and type 2 diabetes. Apigenin and luteolin were identified in our U-2 OS (human osteosarcoma) cell screening assay for micronutrients triggering rapid intracellular translocation of the forkhead box transcription factor O1 (FOXO1), an important mediator of insulin signal transduction. Insulin reversed the translocation of FOXO1 as shown by live cell imaging. The impact on the expression of target genes was evaluated in HepG2 (human hepatoma) cells. The mRNA-expression of the gluconeogenic enzymes phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pc), the lipogenic enzymes fatty-acid synthase (FASN) and acetyl-CoA-carboxylase (ACC) were down-regulated by both flavones with smaller effective dosages of apigenin than for luteolin. PKB/AKT-, PRAS40-, p70S6K-, and S6-phosphorylation was reduced by apigenin and luteolin but not that of the insulin-like growth factor receptor IGF-1R by apigenin indicating a direct inhibition of the PKB/AKT-signaling pathway distal to the IGF-1 receptor. N-acetyl-L-cysteine did not prevent FOXO1 nuclear translocation induced by apigenin and luteolin, suggesting that these flavones do not act via oxidative stress. The roles of FOXO1, FOXO3a, AKT, sirtuin1 (SIRT1), and nuclear factor (erythroid-derived2)-like2 (NRF2), investigated by siRNA knockdown, showed differential patterns of signal pathways involved and a role of NRF2 in the inhibition of gluconeogenic enzyme expression. We conclude that these flavones show an antidiabetic potential due to reduction of gluconeogenic and lipogenic capacity despite inhibition of the PKB/AKT pathway which justifies detailed investigation in vivo.

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<![CDATA[Effect of a Brown Rice Based Vegan Diet and Conventional Diabetic Diet on Glycemic Control of Patients with Type 2 Diabetes: A 12-Week Randomized Clinical Trial]]> https://www.researchpad.co/article/5989da69ab0ee8fa60b92698

Objective

Several intervention studies have suggested that vegetarian or vegan diets have clinical benefits, particularly in terms of glycemic control, in patients with type 2 diabetes (T2D); however, no randomized controlled trial has been conducted in Asians who more commonly depend on plant-based foods, as compared to Western populations. Here, we aimed to compare the effect of a vegan diet and conventional diabetic diet on glycemic control among Korean individuals.

Materials and Methods

Participants diagnosed with T2D were randomly assigned to follow either a vegan diet (excluding animal-based food including fish; n = 46) or a conventional diet recommended by the Korean Diabetes Association 2011 (n = 47) for 12 weeks. HbA1c levels were measured at weeks 0, 4, and 12, and the primary study endpoint was the change in HbA1c levels over 12 weeks.

Results

The mean HbA1c levels at weeks 0, 4, and 12 were 7.7%, 7.2%, and 7.1% in the vegan group, and 7.4%, 7.2%, and 7.2% in the conventional group, respectively. Although both groups showed significant reductions in HbA1C levels, the reductions were larger in the vegan group than in the conventional group (-0.5% vs. -0.2%; p-for-interaction = 0.017). When only considering participants with high compliance, the difference in HbA1c level reduction between the groups was found to be larger (-0.9% vs. -0.3%). The beneficial effect of vegan diets was noted even after adjusting for changes in total energy intake or waist circumference over the 12 weeks.

Conclusion

Both diets led to reductions in HbA1c levels; however, glycemic control was better with the vegan diet than with the conventional diet. Thus, the dietary guidelines for patients with T2D should include a vegan diet for the better management and treatment. However, further studies are needed to evaluate the long-term effects of a vegan diet, and to identify potential explanations of the underlying mechanisms.

Trial Registration

CRiS KCT0001771

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<![CDATA[Effects of the Mediterranean Diet on Cardiovascular Outcomes—A Systematic Review and Meta-Analysis]]> https://www.researchpad.co/article/5989dadbab0ee8fa60bb9cfa

Background

A Mediterranean dietary pattern is widely recommended for the prevention of chronic disease. We sought to define the most likely effects of the Mediterranean diet on vascular disease and mortality.

Methods

We searched MEDLINE, EMBASE and the Cochrane Central Register without language restriction for randomized controlled trials comparing Mediterranean to control diets. Data on study design, patient characteristics, interventions, follow-up duration, outcomes and adverse events were sought. Individual study relative risks (RR) were pooled to create summary estimates.

Results

Six studies with a total of 10950 participants were included. Effects on major vascular events (n = 477), death (n = 693) and vascular deaths (n = 315) were reported for 3, 5 and 4 studies respectively. For one large study (n = 1000) there were serious concerns about the integrity of the data. When data for all studies were combined there was evidence of protection against major vascular events (RR 0.63, 95% confidence interval 0.53–0.75), coronary events (0.65, 0.50–0.85), stroke (0.65, 0.48–0.88) and heart failure (0.30, 0.17–0.56) but not for all-cause mortality (1.00, 0.86–1.15) or cardiovascular mortality (0.90, 0.72–1.11). After the study of concern was excluded the benefit for vascular events (0.69, 0.55–0.86) and stroke (0.66, 0.48–0.92) persisted but apparently positive findings for coronary events (0.73, 0.51–1.05) and heart failure (0.25, 0.05–1.17) disappeared.

Conclusion

The Mediterranean diet may protect against vascular disease. However, both the quantity and quality of the available evidence is limited and highly variable. Results must be interpreted with caution.

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