scholarly journals Leptin and Adiponectin Signaling Pathways Are Involved in the Antiobesity Effects of Peanut Skin Extract

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Lan Xiang ◽  
Qiaobei Wu ◽  
Lihong Cheng ◽  
Kaiyue Sun ◽  
Jing Li ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Metabolic Disorders ◽  
Leptin Receptor ◽  
Skin Extract ◽  
Mass Ratio ◽  
Fat Tissue ◽  
Thrombocytopenic Purpura ◽  
Peanut Skin ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes

Excessive food intake and metabolic disorder promote obesity and diabetes. In China, peanut skin is used as a herbal medicine to treat hemophilia, thrombocytopenic purpura, and hepatic hemorrhage. In the present study, we demonstrated that peanut skin extract (PSE) safely reduced appetite, body weight, fat tissue, plasma TG and TC, and blood glucose level in mice with diet-induced obesity (DIO). Moreover, the leptin/leptin receptor/neuropeptide Y (NPY) and adiponectin signaling pathways involved in the antiobesity effects of PSE are confirmed through leptin and adiponectin overexpression and leptin receptor silencing in mice. PSE consisted of oligosaccharide and polyphenol in a mass ratio of 45 : 55, and both parts were important for the antiobesity function of PSE. Our results suggested that PSE can be developed as functional medical food to treat metabolic disorders and obesity.

scholarly journals Endospanin 1 Determines the Balance of Leptin-Regulated Hypothalamic Functions

2018 ◽  
Vol 108 (2) ◽  
pp. 132-141
Author(s):  
Clara Roujeau ◽  
Ralf Jockers ◽  
Julie Dam
Keyword(s):  
Signaling Pathways ◽  
Intracellular Trafficking ◽  
Leptin Receptor ◽  
Leptin Resistance ◽  
Human Obesity ◽  
Leptin Signaling ◽  
Diet Induced Obesity ◽  
Important Regulator ◽  
Neuronal Plasma Membrane ◽  
Underlying Mechanisms

Endospanin 1 (Endo1), a protein encoded in humans by the same gene than the leptin receptor (ObR), and increased by diet-induced obesity, is an important regulator of ObR trafficking and cell surface exposure, determining leptin signaling strength. Defective intracellular trafficking of the leptin receptor to the neuronal plasma membrane has been proposed as a mechanism underlying the development of leptin resistance observed in human obesity. More recently, Endo1 has emerged as a mediator of “selective leptin resistance.” The underlying mechanisms of the latter are not completely understood, but the possibility of differential activation of leptin signaling pathways was suggested among others. In this respect, the expression level of Endo1 is crucial for the appropriate balance between different leptin signaling pathways and leptin functions in the hypothalamus and is likely participating in selective leptin resistance for the control of energy and glucose homeostasis.

scholarly journals Endothelial leptin receptor mutation provides partial resistance to diet-induced obesity

2012 ◽  
Vol 112 (8) ◽  
pp. 1410-1418 ◽  
Author(s):  
Weihong Pan ◽  
Hung Hsuchou ◽  
Germaine G. Cornelissen-Guillaume ◽  
Bhavvani Jayaram ◽  
Yuping Wang ◽  
...  
Keyword(s):  
Body Weight ◽  
Partial Resistance ◽  
Heat Dissipation ◽  
Leptin Receptor ◽  
Wild Type ◽  
Blood Concentrations ◽  
Leptin Signaling ◽  
Metabolic Chamber ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes

Leptin, a polypeptide hormone produced mainly by adipocytes, has diverse effects in both the brain and peripheral organs, including suppression of feeding. Other than mediating leptin transport across the blood-brain barrier, the role of the endothelial leptin receptor remains unclear. We recently generated a mutant mouse strain lacking endothelial leptin receptor signaling, and showed that there is an increased uptake of leptin by brain parenchyma after its delivery by in situ brain perfusion. Here, we tested the hypothesis that endothelial leptin receptor mutation confers partial resistance to diet-induced obesity. These ELKO mice had similar body weight and percent fat as their wild-type littermates when fed with rodent chow, but blood concentrations of leptin were significantly elevated. In response to a high-fat diet, wild-type mice had a greater gain of body weight and fat than ELKO mice. As shown by metabolic chamber measurement, the ELKO mice had higher oxygen consumption, carbon dioxide production, and heat dissipation, although food intake was similar to that of the wild-type mice and locomotor activity was even reduced. This indicates that the partial resistance to diet-induced obesity was mediated by higher metabolic activity in the ELKO mice. Since neuronal leptin receptor knockout mice show obesity and diabetes, the results suggest that endothelial leptin signaling shows opposite effects from that of neuronal leptin signaling, with a facilitatory role in diet-induced obesity.

scholarly journals Hijacking Dorsal Raphe to Improve Metabolism and Depression-like Behaviors via BDNF Gene Transfer in Mice

2021 ◽  
Author(s):  
Jianbo Xiu ◽  
Rongrong Han ◽  
Zeyue Liu ◽  
Jiayu Li ◽  
Shu Liu ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Metabolic Disorders ◽  
Dorsal Raphe ◽  
Mild Stress ◽  
Bdnf Gene ◽  
Diet Induced Obesity ◽  
Serotonergic Activity ◽  
Obesity And Diabetes ◽  
Diabetes And Obesity ◽  
Dorsal Raphé

Moods and metabolism modulate each other. High comorbidity of depression and metabolic disorders such as diabetes and obesity poses a great challenge to treat such condition. Here we report the therapeutic efficacy of brain-derived neurotrophic factor (BDNF) by gene transfer in the dorsal raphe nucleus (DRN) in a chronic unpredictable mild stress model of depression (CUMS) and models of diabetes and obesity. In CUMS, BDNF-expressing mice displayed antidepressant- and anxiolytic-like behaviors, which are associated with augmented serotonergic activity. Both in the diet-induced obesity model (DIO) and in <i>db/db</i> mice，BDNF ameliorated obesity and diabetes, which may be mediated by enhanced sympathetic activity, not involving DRN serotonin. Chronic activation of DRN neurons via chemogenetic tools produced similar effects as BDNF in DIO mice. These results established the DRN as a key nexus in regulating depression-like behaviors and metabolism, which can be exploited to combat comorbid depression and metabolic disorders via BDNF gene transfer.

scholarly journals Hijacking Dorsal Raphe to Improve Metabolism and Depression-like Behaviors via BDNF Gene Transfer in Mice

2021 ◽  
Author(s):  
Jianbo Xiu ◽  
Rongrong Han ◽  
Zeyue Liu ◽  
Jiayu Li ◽  
Shu Liu ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Metabolic Disorders ◽  
Dorsal Raphe ◽  
Mild Stress ◽  
Bdnf Gene ◽  
Diet Induced Obesity ◽  
Serotonergic Activity ◽  
Obesity And Diabetes ◽  
Diabetes And Obesity ◽  
Dorsal Raphé

Moods and metabolism modulate each other. High comorbidity of depression and metabolic disorders such as diabetes and obesity poses a great challenge to treat such condition. Here we report the therapeutic efficacy of brain-derived neurotrophic factor (BDNF) by gene transfer in the dorsal raphe nucleus (DRN) in a chronic unpredictable mild stress model of depression (CUMS) and models of diabetes and obesity. In CUMS, BDNF-expressing mice displayed antidepressant- and anxiolytic-like behaviors, which are associated with augmented serotonergic activity. Both in the diet-induced obesity model (DIO) and in <i>db/db</i> mice，BDNF ameliorated obesity and diabetes, which may be mediated by enhanced sympathetic activity, not involving DRN serotonin. Chronic activation of DRN neurons via chemogenetic tools produced similar effects as BDNF in DIO mice. These results established the DRN as a key nexus in regulating depression-like behaviors and metabolism, which can be exploited to combat comorbid depression and metabolic disorders via BDNF gene transfer.

scholarly journals Mixture of Peanut Skin Extract and Fish Oil Improves Memory in Mice via Modulation of Anti-Oxidative Stress and Regulation of BDNF/ERK/CREB Signaling Pathways

Nutrients ◽  
2016 ◽  
Vol 8 (5) ◽  
pp. 256 ◽  
Author(s):  
Lan Xiang ◽  
Xue-Li Cao ◽  
Tian-Yan Xing ◽  
Daisuke Mori ◽  
Rui-Qi Tang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fish Oil ◽  
Signaling Pathways ◽  
Skin Extract ◽  
Peanut Skin

The outer membrane protein Amuc_1100 of Akkermansia muciniphila promotes intestinal 5-HT biosynthesis and extracellular availability through TLR2 signalling

2021 ◽  
Author(s):  
Junchao Wang ◽  
Wenjuan Xu ◽  
Rongjuan Wang ◽  
Rongrong Cheng ◽  
Zhengquan Tang ◽  
...  
Keyword(s):  
Membrane Protein ◽  
Outer Membrane ◽  
Outer Membrane Protein ◽  
Metabolic Disorders ◽  
Therapeutic Effects ◽  
Akkermansia Muciniphila ◽  
Intestinal Mucus ◽  
Obesity And Diabetes

Akkermansia muciniphila is a probiotic inhabiting host intestinal mucus layers and displays evident easing or therapeutic effects on host enteritis and metabolic disorders such as obesity and diabetes. The outer...

scholarly journals PWD/PhJ and WSB/EiJ Mice Are Resistant to Diet-Induced Obesity But Have Abnormal Insulin Secretion

Endocrinology ◽  
2011 ◽  
Vol 152 (8) ◽  
pp. 3005-3017 ◽  
Author(s):  
Katie T. Y. Lee ◽  
Subashini Karunakaran ◽  
Maggie M. Ho ◽  
Susanne M. Clee
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Large Scale ◽  
Mouse Strains ◽  
Second Phase ◽  
Fasting Insulin ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes

Recently, novel inbred mouse strains that are genetically distinct from the commonly used models have been developed from wild-caught mice. These wild-derived inbred strains have been included in many of the large-scale genomic projects, but their potential as models of altered obesity and diabetes susceptibility has not been assessed. We examined obesity and diabetes-related traits in response to high-fat feeding in two of these strains, PWD/PhJ (PWD) and WSB/EiJ (WSB), in comparison with C57BL/6J (B6). Young PWD mice displayed high fasting insulin levels, although they had normal insulin sensitivity. PWD mice subsequently developed a much milder and delayed-onset obesity compared with B6 mice but became as insulin resistant. PWD mice had a robust first-phase and increased second-phase glucose-stimulated insulin secretion in vivo, rendering them more glucose tolerant. WSB mice were remarkably resistant to diet-induced obesity and maintained very low fasting insulin throughout the study. WSB mice exhibited more rapid glucose clearance in response to an insulin challenge compared with B6 mice, consistent with their low percent body fat. Interestingly, in the absence of a measurable in vivo insulin secretion, glucose tolerance of WSB mice was better than B6 mice, likely due to their enhanced insulin sensitivity. Thus PWD and WSB are two obesity-resistant strains with unique insulin secretion phenotypes. PWD mice are an interesting model that dissociates hyperinsulinemia from obesity and insulin resistance, whereas WSB mice are a model of extraordinary resistance to a high-fat diet.

scholarly journals High-Fat Diet and Age-Dependent Effects of IgA-Bearing Cell Populations in the Small Intestinal Lamina Propria in Mice

2021 ◽  
Vol 22 (3) ◽  
pp. 1165
Author(s):  
Yuta Sakamoto ◽  
Masatoshi Niwa ◽  
Ken Muramatsu ◽  
Satoshi Shimo
Keyword(s):  
Immune Function ◽  
Lamina Propria ◽  
High Fat Diet ◽  
Immunoglobulin A ◽  
Immune Functions ◽  
High Fat ◽  
Intestinal Villi ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes

Several studies highlighted that obesity and diabetes reduce immune function. However, changes in the distribution of immunoglobins (Igs), including immunoglobulin-A (IgA), that have an important function in mucosal immunity in the intestinal tract, are unclear. This study aimed to investigate the impaired immune functions in the context of a diet-induced obese murine model via the assessment of the Igs in the intestinal villi. We used mice fed a high-fat diet (HFD) from four to 12 or 20 weeks of age. The distributions of IgA, IgM, and IgG1 were observed by immunohistochemistry. Interestingly, we observed that IgA was immunolocalized in many cells of the lamina propria and that immunopositive cells increased in mice aged 12 to 20 weeks. Notably, mice fed HFD showed a reduced number of IgA-immunopositive cells in the intestinal villi compared to those fed standard chow. Of note, the levels of IgM and IgG1 were also reduced in HFD fed mice. These results provide insights into the impaired mucosal immune function arising from diet-induced obesity and type 2 diabetes.

scholarly journals Ancient Origins and Evolutionary Conservation of Intracellular and Neural Signaling Pathways Engaged by the Leptin Receptor

Endocrinology ◽  
2014 ◽  
Vol 155 (11) ◽  
pp. 4202-4214 ◽  
Author(s):  
Melissa Y. Cui ◽  
Caroline K. Hu ◽  
Chris Pelletier ◽  
Adam Dziuba ◽  
Rose H. Slupski ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Leptin Receptor ◽  
Evolutionary Conservation ◽  
Neural Signaling

LDL receptor but not apolipoprotein E deficiency increases diet-induced obesity and diabetes in mice

2002 ◽  
Vol 282 (1) ◽  
pp. E207-E214 ◽  
Author(s):  
Sandra A. Schreyer ◽  
Cynthia Vick ◽  
Theodore C. Lystig ◽  
Paul Mystkowski ◽  
Renée C. LeBoeuf
Keyword(s):  
Apolipoprotein E ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Wild Type ◽  
Glucose Levels ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes ◽  
Glucose And Lipid Homeostasis

The aim of this study was to determine whether phenotypes associated with type 2 diabetes are altered in dyslipidemic obese mice. C57BL/6 wild-type, low-density lipoprotein (LDL) receptor-deficient (LDLR−/−), and apolipoprotein E-deficient (apoE−/−) mice were fed a high-fat, high-carbohydrate diet (diabetogenic diet), and the development of obesity, diabetes, and hypertriglyceridemia was examined. Wild-type mice became obese and developed hyperglycemia, but not hypertriglyceridemia, in response to this diet. LDLR−/− mice fed the diabetogenic diet became more obese than wild-type mice and developed severe hypertriglyceridemia and hyperleptinemia. Surprisingly, glucose levels were only modestly higher and insulin levels and insulin-to-glucose ratios were not strikingly different from those of wild-type mice. In contrast, diabetogenic diet-fed apoE−/− mice were resistant to changes in glucose and lipid homeostasis despite becoming obese. These data suggest that modifications in lipoprotein profiles associated with loss of the LDL receptor or apoE function have profound and unique consequences on susceptibility to diet-induced obesity and type 2 diabetic phenotypes.

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