ResearchPad - adipose-tissue-biology-and-obesity https://www.researchpad.co Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[SUN-586 CXCR2 Repression by Glucocorticoids in Adipose Tissue]]> https://www.researchpad.co/article/elastic_article_8741 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.

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<![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]]> https://www.researchpad.co/article/elastic_article_8594 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.

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<![CDATA[SAT-LB105 A Transcribed Ultraconserved Noncoding RNA, Uc.336-As, Promotes White to Brown Conversion in 3T3-L1 Cells]]> https://www.researchpad.co/article/elastic_article_8553 Brown adipose tissue (BAT) has gained its popularity since it shows great potential in counteracting obesity and metabolic diseases development. Transcribed ultraconserved regions (T-UCRs), a novel class of long non-coding RNA (lncRNAs), have been implicated in regulating diverse biological processes, including the process of white fat browning. However, the functional and mechanistic details of T-UCRs in the browning process are poorly understood. Here, we identified that a T-UCR, uc.336-as, played an important role during the browning process. Uc.336-as was significantly elevated during browning process induced by glucagon-like peptide-1 receptor agonist (exendin-4) or β3-adrenergic agonist (CL316,243). Overexpression of uc.336-as reduces the differentiation of 3T3-L1 preadipocytes into white adipocytes (inhibited lipid accumulation and decreased the expression of several adipogenesis markers) and induces brown characteristics during differentiation of 3T3-L1 preadipocytes (spurred browning adipocytes phenotypes and increased the expression of the browning associated genes). Moreover, we found that uc.336-as inhibited adipogenesis and promoted browning process via influencing the serine/threonine kinase (AKT)-mammalian target of rapamycin (mTOR) axis, an essential signal pathway in adipocyte metabolism. Taken together, our data show that uc.336-as acts as a negative regulator in white adipocyte differentiation and promotes the browning process, suggesting a potential therapeutic role for uc.336-as in controlling obesity.

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<![CDATA[SUN-591 PAPP-A Inhibition - a Novel Anti-Obesity Therapeutic Approach]]> https://www.researchpad.co/article/elastic_article_7101 Background: Adipose tissue is a heterogeneous endocrine organ with tremendous capability for expansion. The antithetical pathogenicity of visceral adipose tissue (VAT), compared to subcutaneous adipose tissue (SAT), has been linked to the metabolic stress of enlarging mature adipocytes and a limited ability to recruit new adipocytes. One of the major distinguishing features of VAT preadipocytes is the high expression of Pregnancy Associated Plasma Protein–A (PAPP-A) when compared to SAT. PAPP-A is a zinc metalloprotease that is secreted, and can associate with the cell surface in an autocrine or paracrine fashion. It is the only known physiological IGFBP-4 (Insulin-like Growth Factor Binding Protein) protease. It cleaves the IGF/IGFBP-4 complex, releasing IGF, making it more bio-available for receptor engagement and downstream signaling. The role of IGFs in adipogenic differentiation is well established. While there is quantitative depot-specific variability in PAPP-A expression among preadipocytes, mature adipocytes do not express any PAPP-A. These findings suggest that there may be a relationship between PAPP-A inhibition and adipogenic differentiation and maturation. Similar to human VAT, PAPP-A expression is highest in visceral fat in murine models. The PAPP-A KO mice, when fed a high fat diet, showed restrained visceral adiposity and decreased visceral adipocyte size, suggesting that PAPP-A could regulate adipogenesis locally in tissues that express high PAPP-A.

Hypothesis: PAPP-A inhibition is a novel anti-obesity treatment strategy. Methods/Results: We fed 20 male and 20 female wild type mice 42% high fat diet (HFD) starting at 10 weeks of age. Concomitantly, we treated 10 mice in each group with either mAb-PA1/41 (a PAPP-A neutralizing monoclonal antibody) or IgG2a (control isotope), intraperitoneally at a dose of 30 mg/kg weekly for the duration of the HFD. At the end of 15 weeks, the mice were sacrificed and the adipose tissue, serum and solid organs were harvested.

Compared to the control (IgG2a) mice, the mAb-PA1/41 treated male and female mice gained 40% less weight (P = 0.03) and had smaller visceral fat depots (mesenteric and pericardial). Also, when we looked at individual adipocyte size, the drug treated mice had 45% smaller mesenteric adipocytes (P = 0.002) and 44% smaller pericardial adipocytes (P= 0.003). Also, the visceral depots in the drug treated mice had 30% more cells (P = 0.006). In both groups, there was decreased liver lipid content (P=0.005). The mAb-PA1/41 treatment had no significant effect on subcutaneous fat depots.

Conclusion: Pharmacologic inhibition of PAPP-A decreased weight gain, visceral fat depot weight, visceral adipocyte size, hepatic lipid deposition and increased visceral adipocyte cell number in both male and female mice that were fed a high fat diet.

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<![CDATA[SAT-LB103 Glucose-Dependent Insulinotropic Polypeptide Promotes Proliferation, Inhibits Apoptosis and Modifies Adipogenesis in Human Omental Adipose-Derived Stem Cells]]> https://www.researchpad.co/article/elastic_article_6881 Increased visceral fat correlates with a high risk of morbidity and mortality from diabetes and other metabolic diseases. To cope with changes of nutritional status, the adipose tissue undergoes dynamic remodeling, during which adipose derived stem cells (ADSCs) participate through cell proliferation and adipogenic differentiation into mature adipocytes. Besides, beige adipocytes formation from ADSCs, to dissipate energy as heat in mitochondrial via uncoupling protein1 (UCP1) has been proved to improve energy expenditure. Thus, modifying adipose remodeling and promoting beige adipogenesis of ADSCs in visceral fat bring much metabolic benefits. Newly listed LY3298176, an agonist targeted on glucose-dependent insulinotropic polypeptide (GIP) /glucagon-like peptide-1 (GLP-1) receptor, shows outstanding effect of reducing glucose and weight. Due to superior efficacy in dual-target agonist to GLP-1 monotherapy, and the unknown role of GIP in human visceral adipose, we aimed to clarify GIP’s role in undifferentiated ADSCs in vivo. We selected cell model derived from abdominal omental adipose tissue by obtaining ADSCs via primary culture from patients, because of wide-distributed GIP receptors in fat, and the dominant role of abdominal fat in metabolism. Then the cells were allowed to proliferate, or differentiate into adipocytes in the differentiation medium (DM), with or without co-treated with GIP or GIP3-42 (GIP receptor antagonist), followed by subsequently measurement. CCK-8, EdU incorporation, and cell cycle analysis were conducted to assess cellular proliferation. Annexin V FITC/PI stain, TUNEL and cleaved caspase3 detection were performed to evaluate apoptosis. The related signaling pathway was measured by Western blot and the validation was conducted by using pathway inhibitors followed with the above proliferation and apoptosis analysis. Besides, at the early stage of adipogenesis, mitotic clonal expansion (MCE) was reflected by cell cycle detection. Western blot analysis, quantitative real time-PCR (qRT-PCR), and Oil Red O staining were performed to evaluate adipogenesis. We found that GIP facilitated ADSCs viability and DNA synthesis, accelerated cell cycle progress and reduced palmitate-induced apoptosis by promoting phosphorylation of ERK1/2, AKT, PKA and AMPK. We further confirmed that ADSCs after confluence underwent MCE once induced by DM. GIP also modified adipogenesis by accelerating MCE, upregulating core transcription factor (PPARγ and C/EBPα), increasing beige-related markers (UCP1, PGC1α, PRDM16, et al) while suppressing white-related genes (ZFP423 and TLE3). In summary, we illustrated the efficacies of GIP on proliferation, apoptosis and adipogenesis (especially the beige adipocyte formation) of ADSCs, providing evidence of the additional metabolic benefits of GIP/GLP-1 dual-target agonist over GLP-1 agonist monotherapy in vivo.

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<![CDATA[SAT-587 Molecular Markers of Beige Adipose Following ESR1 Knockdown in the Mediobasal Hypothalamus of Adult Female Rhesus Monkeys]]> https://www.researchpad.co/article/elastic_article_6873 Our studies in female marmoset monkeys show that the ablation of ovarian estradiol (E2) production fails to alter energy homeostasis or body fat accumulation. Peripheral E2 may therefore not play a crucial role in metabolic regulation in female primates. shRNA-mediated knockdown of ESR1 expression in the hypothalamic ventromedial nucleus (VMN) in adult female rodents, however, induces obesity and suggests ESR1 is a hypothalamic target for E2 regulation of energy homeostasis, and likely mediates thermogenesis in brown/beige adipose depots. In female primates, including humans, the hypothalamic estrogen receptor mediating metabolic regulation is unknown. To test the hypothesis that ESR1 mediates female primate regulation of energy homeostasis, 11 ovary intact, adult female rhesus macaques, pair housed with female peers, received five 12µl MRI-guided MBH infusions into the rostral-to-caudal extent of both right and left VMN. Each infusion comprised a gadolinium contrast agent and ~3–4 x 1010 adeno-associated virus 8 (AAV8) particles containing either an shRNA specific for ESR1 (n=6, ERaKD) or scrambled shRNA (n=5, control). Mid-surgery MRI scans identified targeting accuracy. ~ 1.5 yrs following AAV8 infusion, pronounced gain in BMI enabled conversion of 83% of ERaKD females to overweight/obese compared to 20% of controls (p=0.08). Percent increase in BMI remained intermittently greater (p<0.05) than controls thereafter. Adipose depots were harvested at necropsy ~2.5–3 yrs following treatment. Total RNA was isolated using the Qiagen AllPrep DNA/RNA/miRNA Universal kit. RNA was reverse transcribed with High-Capacity cDNA Reverse Transcription kit (Applied Biosystems). All quantitative real-time PCR (qRT-PCR) were performed on a StepOnePlus System using Power SYBR Green master mix (Applied Biosystems). Primer sequences were designed using NCBI Primer-Blast. Expression of TATA-box binding protein (TBP) was used as the internal control housekeeping gene. The relative expression of target genes was measured using the comparative cycle threshold (Ct) method with results expressed as target mRNA expression relative to TBP using the formula 2^-delta Ct. Upper body beige adipose represents an organ system in primates, including humans, involved in thermogenesis. Axillary beige adipose depots in ERaKD females, however, did not exhibit significantly diminished gene expression for selected markers of beige adipocytes, including PAT2, CD137 and C/EBPβ, compared to control females. More crucially, thermogenically relevant UCP1 expression also did not differ between ERaKD females and controls. Taken together, these results suggest that knockdown of VMN ESR1 in adult female monkeys, while inducing modest weight gain after 1.5 years, may not markedly alter beige adipose gene expression of initially selected thermogenically relevant genes.

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<![CDATA[SAT-588 Role of Adipose Tissue in Reproduction, Mammary Gland Development, Function and Cancer]]> https://www.researchpad.co/article/elastic_article_6718 To investigate the role of adipose tissue in the function of the mammary gland (MG) and reproductive system, we have examined lipodystrophic (LD) mice. LD mice of both sexes are sterile, but fertility was restored in both sexes with leptin injections. In addition, leptin was only needed for initial stages of pregnancy and not for parturition. A transplant of mouse embryonic fibroblasts (MEFs) led to the formation of an ectopic fat pad which also rescued the fertility in both sexes. However, pups born to rescued LD mothers died shortly after birth. We therefore examined the mammary glands of these mothers. MGs from LD mice were rudimentary and lacked terminal end buds. Leptin-injected and MEF rescued LD mice were able to become pregnant, showed normal pregnancy-associated glandular proliferation despite a smaller glandular area, were able to produce a small amount of milk that had grossly normal content of milk proteins and neutral lipids, but could not sustain pups to weaning. In order to separate the individual requirements for 1) adipokines such as leptin, 2) estradiol, and 3) epithelial-adipocyte interactions, we performed a series of experiments with both LD and ob (leptin-deficient) mice that received either estradiol or preadipocyte transplant. The resulting fat pad did not rescue the defect in MG development in LD mice. The defect also was not rescued with estradiol pellets. Ob/ob mice, like LD mice, lack leptin and estradiol, but retain adipose tissue. Ob mice have defective MG development. However, in striking contrast to LD mice, reconstitution of a WT fat pad in ob mice rescued the defect in MG development. Estradiol treatment did not rescue MG development in ob mice. Therefore direct interaction between mammary gland epithelia and adipocytes is a requirement for full invasion and expansion of the gland during puberty, but is not required for glandular proliferation during pregnancy and milk production.

Given that excess adipose tissue is a risk factor for breast cancer we wanted to determine if breast cancer was affected by the absence of adipose tissue. LD mice were bred to MMTV-PyMT mice that develop spontaneous breast cancer. Remarkably, LD PyMT+ mice had accelerated growth of primary tumors compared to WT PyMT+ mice. Using our MEF transplant model future studies will be directed to understanding whether the accelerated breast cancer growth is due to loss of adipokines or altered epithelial-stromal interactions.

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<![CDATA[SUN-590 27-Hydroxycholesterol Triggers the Whitening of Brown Adipose Tissue]]> https://www.researchpad.co/article/elastic_article_6714 27-Hydroxycholesterol (27HC) is the most abundant oxysterol in circulation and metabolized by a P450 enzyme CYP7B1. Its levels closely correspond to those of cholesterol in the body. In addition, previously it was found that 27HC is an endogenous selective estrogen receptor modulator (SERM), which links cholesterol metabolism to estrogen receptor actions (1). Brown adipose tissue (BAT) is the primary source of energy expenditure and energy homeostasis, as well as body temperature maintenance. While previously it was believed that BAT activity is limited to neonates and young children, it is now recognized that BAT is also active in adult humans and its function is impaired by metabolic diseases such as obesity. BAT is also a secretory organ and produces brown adipokines, although the exact function of BAT and adipokines from this tissue in obesity has not been completely understood. Recently, it was reported that 27HC plays an important role in obesity and augments body weight gain in response to a high fat, high cholesterol (HFHC) diet by increasing pre-adipocyte population in the white adipose tissue. 27HC mimics the effects by HFHC diet-feeding on white adipose tissue, such as promoting the inflammation and macrophage infiltration (2). In this study, we explored the effect of 27HC on BAT morphology and function. First, we compared the morphology of BAT from wild-type mice and Cyp7b1-/- mice that have elevated levels of 27HC using H&E staining. Interestingly, brown adipocytes from Cyp7b1-/- mice were larger in cell size than those from wild-type mice, and the cells were mostly unilocular compared to the multilocular cells from wild-type mice, indicating the transition toward a “whitening” phenotype. Next, We treated mice fed a normal chow or a HFHC diet with 27HC or vehicle control for 8 weeks to examine the direct effect by 27HC on BAT. Similar to the phenotype in Cyp7b1-/-mice, 27HC increased the “whitening” of BAT regardless of the diet. We also determined the gene expression of brown adipocyte markers such as UCP1, PGC1a, and DIO2, and found that 27HC significantly decreased the expression of the BAT markers regardless of the diet, confirming the “whitening” observed in the morphology. Moreover, the energy expenditure in mice treated with 27HC was decreased compared to the vehicle control on a HFHC diet, suggesting that 27HC also alters BAT function. These results show that 27HC causes the whitening of BAT, and shed light on the important role of 27HC in brown adipose tissue function. Future experiments will be warranted toward further understanding of the role of 27HC in BAT function. Reference:(1) Umetani, Michihisa, et al. Nature medicine 13.10 (2007): 1185. (2) Asghari, Arvand, et al. Endocrinology 160.10 (2019): 2485-2494.

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<![CDATA[SUN-LB106 The Transcriptomic Evidences on Role of Abdominal Visceral vs. Subcutaneous Adipose Tissue in the Pathophysiology of Diabetes in Asian Indian Indicates the Involvement of Both]]> https://www.researchpad.co/article/N190ded62-2a0d-440b-a78f-243f7aefb42f 25%). Moreover, 12 out of 16 significantly enriched pathways in VAT were among the top 20 pathways in SAT. GSEA in diabetics: VAT vs SAT: None of the gene sets were found significant at FDR < 25% which substantiated our hypothesis that overall pathophysioloigcal alteration in both depots are similar. WGCNA for statistical comparison of VAT and SAT depots The correlation between measures of average gene expression and overall connectivity between both depots was significantly positive. Several modules of co-expressed genes in both VAT and SAT showed positive as well as negative correlation with various intermediate phenotypic traits of diabetes. In both depots they enriched several pathways otherwise known to be associated with pathological adipose tissue like inflammation, adipogenesis etc.ConclusionsIn Asian Indians, diabetes pathology inflicts similar molecular alternations in VAT and SAT, which are more intense in the former. The role of both adipose depots in the pathophysiology of diabetes is along similar lines and they enrich several molecular pathways which are otherwise known to be implicated in pathological adipose tissue. ]]> <![CDATA[SUN-584 Micrornas in Brown and White Adipocytes]]> https://www.researchpad.co/article/N93493193-97db-431b-af15-3cc07acc1def <![CDATA[SUN-589 MED1 Is a Lipogenesis Coactivator Required for Postnatal Adipose Tissue Expansion]]> https://www.researchpad.co/article/Nf4129607-065a-43d3-9bbc-f46a48720867 <![CDATA[SUN-587 IDH1-Dependent Alpha-KG Regulates Brown Fat Differentiation and Function by Modulating Histone Methylation]]> https://www.researchpad.co/article/N47f9d4c1-362d-4827-ab74-9ce654734727 <![CDATA[SAT-LB106 Metabolic and Brown Adipose Tissue-Specific Effects of the Novel Non-Steroidal Mineralocorticoid Receptor Antagonist Finerenone in a Mouse Model of Diet-Induced Obesity]]> https://www.researchpad.co/article/Na4203dd0-c8f9-4458-8e6b-c3e96896d147 <![CDATA[SAT-LB107 Insulin Sensing by Astrocytes Is Critical for Normal Thermogenesis and Body Temperature Regulation]]> https://www.researchpad.co/article/Neef51046-5202-410e-aa31-b57b49568c99 <![CDATA[SUN-LB102 Development of a Conceptual Model to Present the Impacts of Obesity on Physical Functioning]]> https://www.researchpad.co/article/Nb05cb7bc-0e2b-4b0a-9a55-429b10a0f915 <![CDATA[SUN-585 Associations Between UCP1(rs1800592),UCP2(rs6593366) and UCP3(rs1800849) with Fasting Glucose, Body Mass Index, and Energy Expenditure]]> https://www.researchpad.co/article/N04b4147f-7a58-4d40-a520-ee2b6619dd13 30kg/m2 and 100 subjects with BMI between18.5 -24.9 kg/m2, aged 20 to 50 years. Anthropometric data were recorded and the REE was measure for indirect calorimetric. Fasting glucose and lipid profile were assessed. Leptin, insulin and acylated-ghrelin were quantified by ELISA. Genomic DNA was extracted using comercial kit. Genotyping for three polymorphisms was performed by allelic discrimination using Taqman probes. Results: All the three polymorphisms of UCPs showed distribution in accordance with Hardy-Weinberg equilibrium. The weight, BMI, glucose, triglycerides, leptin, insulin, HOMA-IR, and REE levels were signitifcantly higher in obese subjects. There was a strong correlation between REE with BMI (r=0.42, p<0.00001) and with insulin levels (r=0.229, p=0.001) in all group. No differences in genotypic and allelic frequencies of rs1800592 UCP-1, rs659366 UCP-2 and rs180084 UCP-3 polymorphisms between obese and lean subjects. No differences among the genotypes rs1800592 UCP-1 and rs1800849 UCP-3 with metabolic variables. In rs659366 UCP-2 polymorhism, the REE and glucose concentrations were lower in carriers of rs659366AA genotype (F=3.11, p=0.046; F=2.97, p=0.053, respectively) in whole group. In obese subjects with rs659366AA UCP-2 genotype, the REE was significantly low (F=4.15, P=0.017). Conclusion. In this work the obese subjects with rs659366AA genotype had low REE. We found low glucose concentrations in the carries of rs659366 AA genotype. ]]> <![CDATA[SUN-LB101 NRF2 Represses Obesity-Associated Adipose Tissue Inflammation in Mice]]> https://www.researchpad.co/article/Nb57a9370-9c0c-4cba-867c-615c73513ebb <![CDATA[SUN-LB100 GDF15 May Be Regulated by Cortisol After Sleeve Bariatric Surgery GDF15 May Be Regulated by Cortisol After Sleeve Bariatric Surgery]]> https://www.researchpad.co/article/N2f8cf500-e8ad-4526-96b2-267e34460fd8 <![CDATA[SAT-LB101 Loss of GLP-2R Signaling Activates Hepatic Stellate Cells and Exacerbates Diet-Induced Steatohepatitis in Mice]]> https://www.researchpad.co/article/Nd887d4d7-ece2-40c8-a751-f7cb5a3a71bf <![CDATA[SAT-LB104 Maternal Non-Nutritive Sweeteners Consumption Perturbs Development of Melanocortin Circuits Causing Long-Term Metabolic Alterations in the Offspring]]> https://www.researchpad.co/article/N3f3f11ff-b03a-4920-bdd1-2a3c684c8dcd