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Jun Huang Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio, USA

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Rita Sharma Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio, USA

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Sohana Siyar Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio, USA

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Vishva Sharma Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio, USA
The Diabetes Institute, Ohio University, Athens, Ohio, USA

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Vishwajeet Puri Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio, USA
The Diabetes Institute, Ohio University, Athens, Ohio, USA

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Kevin Y Lee Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio, USA
The Diabetes Institute, Ohio University, Athens, Ohio, USA

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Studies in humans and mice have determined that distinct subpopulations of adipocytes reside even within individual adipose tissue depots. Previously, our lab defined three white adipocyte subpopulations with stable and unique gene expression profiles, which were termed type 1, 2, and 3 adipocytes, respectively. Our previous studies demonstrated that type 2 adipocytes were highly responsive to the inflammatory cytokine, tumor necrosis factor alpha (TNFα). This study extends these findings to investigate the role of type 2 adipocytes in obesity. We found that treatment with TNFα increased lipolysis specifically in type 2 adipocytes, at least in part, through the reduction of fat-specific protein 27 (FSP27) expression. To assess the physiological role of lipolysis from this adipocyte subpopulation, a type2Ad-hFSP27tg mouse model was generated by overexpressing human FSP27 specifically in type 2 adipocytes. Glucose and insulin tolerance test analysis showed that male type2Ad-hFSP27tg mice on 60% high-fat diet exhibited improved glucose tolerance and insulin sensitivity, with no change in body weight compared to controls. These metabolic changes may, at least in part, be explained by the reduced lipolysis rate in the visceral fat of type2Ad-hFSP27tg mice. Although FSP27 overexpression in primary type 2 adipocytes was sufficient to acutely reduce TNFα-induced apoptosis in vitro, it failed to reduce macrophage infiltration in obesity in vivo. Taken together, these results strongly suggest that type 2 adipocytes contribute to the regulation of lipolysis and could serve as a potential therapeutic target for obesity-associated insulin resistance.

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You-Hua Xu Faculty of Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China
State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China

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Chen-Lin Gao Faculty of Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China
State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China
Department of Endocrinology, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China

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Heng-Li Guo Faculty of Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China
State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China

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Wen-Qian Zhang Faculty of Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China
State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China

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Wei Huang Faculty of Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China
State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China
Department of Endocrinology, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China

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Shan-Shan Tang Faculty of Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China
State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China

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Wen-Jun Gan Faculty of Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China
State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China

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Yong Xu Faculty of Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China
Department of Endocrinology, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China

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Hua Zhou Faculty of Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China
State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China

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Quan Zhu Faculty of Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China
State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Taipa, Macao, China

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Endotoxemia has been recognized to be closely accompanied with type 2 diabetes mellitus (T2DM) and is responsible for many diabetic complications. Recent study suggests the potential role of butyrate, a short-chain fatty acid (SCFA) from microbiota metabolite, on T2DM. Gut-leak is a key event in diabetic-endotoxemia. To investigate if butyrate could ameliorate diabetic-endotoxemia, both in vivo and in vitro experiments were carried out in the present study. The effect of butyrate supplementation on blood HbA1c and inflammatory cytokines were determined in db/db mice; gut barrier integrity and expression of tight junction proteins were investigated both in vivo and in vitro. Oral butyrate administration significantly decreased blood HbA1c, inflammatory cytokines and LPS in db/db mice; inflammatory cell infiltration was reduced, and gut integrity and intercellular adhesion molecules were increased as detected by HE staining, immunohistochemistry and Western blot. By gut microbiota assay, ratio of Firmicutes:Bacteroidetes for gut microbiota was reduced by butyrate. In Caco-2 cells, butyrate significantly promoted cell proliferation, decreased inflammatory cytokines’ secretion, enhanced cell anti-oxidative stress ability and preserved the epithelial monocellular integrity, which was damaged by LPS. The present findings demonstrated that butyrate supplementation could ameliorate diabetic-endotoxemia in db/db mice via restoring composition of gut microbiota and preserving gut epithelial barrier integrity.

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Jun-Ping Wen Department of Endocrinology, Department of Endocrinology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, China
Department of Endocrinology, Department of Endocrinology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, China

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Chune Liu Department of Endocrinology, Department of Endocrinology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, China

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Wen-Kai Bi Department of Endocrinology, Department of Endocrinology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, China

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Ya-Ting Hu Department of Endocrinology, Department of Endocrinology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, China

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Qingshi Chen Department of Endocrinology, Department of Endocrinology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, China

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Huibing Huang Department of Endocrinology, Department of Endocrinology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, China

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Ji-Xing Liang Department of Endocrinology, Department of Endocrinology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, China

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Lian-Tao Li Department of Endocrinology, Department of Endocrinology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, China

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Li-Xiang Lin Department of Endocrinology, Department of Endocrinology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, China

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Gang Chen Department of Endocrinology, Department of Endocrinology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, China

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Adiponectin secreted from adipose tissues plays a role in the regulation of energy homeostasis, food intake, and reproduction in the hypothalamus. We have previously demonstrated that adiponectin significantly inhibited GNRH secretion from GT1-7 hypothalamic GNRH neuron cells. In this study, we further investigated the effect of adiponectin on hypothalamic KISS1 gene transcription, which is the upstream signal of GNRH. We found that globular adiponectin (gAd) or AICAR, an artificial AMPK activator, decreased KISS1 mRNA transcription and promoter activity. Conversely, inhibition of AMPK by Compound C or AMPKα1-SiRNA augmented KISS1 mRNA transcription and promoter activity. Additionally, gAd and AICAR decreased the translocation of specificity protein-1 (SP1) from cytoplasm to nucleus; however, Compound C and AMPKα1-siRNA played an inverse role. Our experiments in vivo demonstrated that the expression of Kiss1 mRNA was stimulated twofold in the Compound C-treated rats and decreased about 60–70% in gAd- or AICAR-treated rats compared with control group. The numbers of kisspeptin immunopositive neurons in the arcuate nucleus region of Sprague Dawley rats mimicked the same trend seen in Kiss1 mRNA levels in animal groups with different treatments. In conclusion, our results provide the first evidence that adiponectin reduces Kiss1 gene transcription in GT1-7 cells through activation of AMPK and subsequently decreased translocation of SP1.

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Yi Jun Desmond Tan Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA
Faculty of Medicine & Health Sciences, UCSI University, Cheras, Kuala Lumpur, Malaysia

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Danielle L Brooks Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Kelly Yin Han Wong Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA
Faculty of Medicine & Health Sciences, UCSI University, Cheras, Kuala Lumpur, Malaysia

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Yuefei Huang Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Jose R Romero Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Jonathan S Williams Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Luminita H Pojoga Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Biologic sex influences the development of cardiovascular disease and modifies aldosterone (ALDO) and blood pressure (BP) phenotypes: females secrete more ALDO, and their adrenal glomerulosa cell is more sensitive to stimulation. Lysine-specific demethylase 1 (LSD1) variants in Africans and LSD1 deficiency in mice are associated with BP and/or ALDO phenotypes. This study, in 18- and 40-week-old wild type (WT) and LSD1+/− mice, was designed to determine whether (1) sex modifies ALDO biosynthetic enzymes; (2) LSD1 deficiency disrupts the effect of sex on these enzymes; (3) within each genotype, there is a positive relationship between ALDO biosynthesis (proximate phenotype), plasma ALDO (intermediate phenotype) and BP levels (distant phenotype); and (4) sex and LSD1 genotype interact on these phenotypes. In WT mice, female sex increases the expression of early enzymes in ALDO biosynthesis but not ALDO levels or systolic blood pressure (SBP). However, enzyme expressions are shifted downward in LSD1+/− females vs males, so that early enzyme levels are similar but the late enzymes are substantially lower. In both age groups, LSD1 deficiency modifies the adrenal enzyme expressions, circulating ALDO levels, and SBP in a sex-specific manner. Finally, significant sex/LSD1 genotype interactions modulate the three phenotypes in mice. In conclusion, biologic sex in mice interacts with LSD1 deficiency to modify several phenotypes: (1) proximal (ALDO biosynthetic enzymes); (2) intermediate (circulating ALDO); and (3) distant (SBP). These results provide entry to better understand the roles of biological sex and LSD1 in (1) hypertension heterogeneity and (2) providing more personalized treatment.

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Ziping Jiang Department of Hand and Foot Surgery, The First Hospital of Jilin University, Changchun, Jilin, China

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Junduo Wu Department of Cardiology, The Second Hospital of Jilin University

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Fuzhe Ma Department of Nephrology, The First Hospital of Jilin University, Changchun, Jilin, China

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Jun Jiang Department of Neurosurgery, The Second Hospital of Shandong University, Jinan, Shandong, China

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Linlin Xu Department of Neurology, The Second Hospital of Shandong University, Jinan, Shandong, China

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Lei Du Department of Nutrition and Food Hygiene, School of Public Health, Shandong University, Jinan, Shandong, China

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Wenlin Huang School of Science and Technology, Georgia Gwinnett College, Lawrenceville, Georgia, USA

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Zhaohui Wang Department of Acupuncture and Tuina, Changchun University of Chinese Medicine, Changchun, Jilin, China

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Ye Jia Department of Diabetes Complications and Metabolism, Diabetes Metabolism Research Institute, Beckman Research Institute of City of Hope, Duarte, California, USA

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Laijin Lu Department of Hand and Foot Surgery, The First Hospital of Jilin University, Changchun, Jilin, China

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Hao Wu Department of Nutrition and Food Hygiene, School of Public Health, Shandong University, Jinan, Shandong, China

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Over a half of the diabetic individuals develop macrovascular complications that cause high mortality. Oxidative stress (OS) promotes endothelial dysfunction (ED) which is a critical early step toward diabetic macrovascular complications. Nuclear factor erythroid 2-related factor 2 (NRF2) is a master regulator of cellular antioxidant defense system and combats diabetes-induced OS. Previously, we found that impaired NRF2 antioxidant signaling contributed to diabetes-induced endothelial OS and dysfunction in mice. The present study has investigated the effect of microRNA-200a (miR-200a) on NRF2 signaling and diabetic ED. In aortic endothelial cells (ECs) isolated from C57BL/6 wild-type (WT) mice, high glucose (HG) reduced miR-200a levels and increased the expression of kelch-like ECH-associated protein 1 (Keap1) – a target of miR-200a and a negative regulator of NRF2. This led to the inactivation of NRF2 signaling and exacerbation of OS and inflammation. miR-200a mimic (miR-200a-M) or inhibitor modulated KEAP1/NRF2 antioxidant signaling and manipulated OS and inflammation under HG conditions. These effects were completely abolished by knockdown of Keap1, indicating that Keap1 mRNA is a major target of miR-200a. Moreover, the protective effect of miR-200a-M was completely abrogated in aortic ECs isolated from C57BL/6 Nrf2 knockout (KO) mice, demonstrating that NRF2 is required for miR-200a’s actions. In vivo, miR-200a-M inhibited aortic Keap1 expression, activated NRF2 signaling, and attenuated hyperglycemia-induced OS, inflammation and ED in the WT, but not Nrf2 KO, mice. Therefore, the present study has uncovered miR-200a/KEAP1/NRF2 signaling that controls aortic endothelial antioxidant capacity, which protects against diabetic ED.

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