The Role of Adiponectin in Maintaining Metabolic Homeostasis

2020 ◽  
Vol 16 (2) ◽  
pp. 95-103 ◽  
Author(s):  
Suleyman Cem Adiyaman ◽  
Muhammet Ozer ◽  
Basak Ozgen Saydam ◽  
Baris Akinci
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Cardiovascular Health ◽  
Metabolic Diseases ◽  
Metabolic Homeostasis ◽  
Glucose And Lipid Metabolism ◽  
Treatment Of Diabetes ◽  
Novel Targets

Background: Adiponectin is an adipocyte-derived cytokine closely associated with obesity, altered body adipose tissue distribution, insulin resistance, and cardiovascular diseases. Introduction: Evidence from animal and human studies demonstrate that adiponectin plays an important role in the regulation of glucose and lipid metabolism. Adiponectin increases insulin sensitivity and improves systemic lipid metabolism. Although research efforts on adiponectin mostly aim towards its endocrine functions, this adipocyte-derived molecule also has profound autocrine and paracrine functions. Conclusion: In this review, our aim is to discuss the role of adiponectin in maintaining metabolic homeostasis and its association with cardiovascular health. The proper identification of these roles is of great importance, which has the potential to identify a wealth of novel targets for the treatment of diabetes and related cardio-metabolic diseases.

scholarly journals Gormony zhirovoy tkani i funktsional'nayaaktivnost' shchitovidnoy zhelezy

2010 ◽  
Vol 7 (4) ◽  
pp. 8-11 ◽  
Author(s):  
N A Petunina ◽  
N E Al'tshuler ◽  
N G Rakova ◽  
L V Trukhina
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Subclinical Hypothyroidism ◽  
Thyroid Dysfunction ◽  
The Impact ◽  
The Relationship ◽  
Tissue Hormones

The review presents a recent data from the literature on the physiologic and pathophysiologic role of adipose tissue hormones (adiponectin, resistin, leptin). The article details the role of adipocytokines in atherogenesis. It also presents the results of studies depicting the relationship between subclinical hypothyroidism, lipid metabolism and insulin resistance as well as the impact of thyroid dysfunction upon the secretion of adipocytokines.

scholarly journals Fibroblast growth factor 21: a regulator of metabolic disease and health span

2017 ◽  
Vol 313 (3) ◽  
pp. E292-E302 ◽  
Author(s):  
Ting Xie ◽  
Po Sing Leung
Keyword(s):  
Lipid Metabolism ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Metabolic Diseases ◽  
Scientific Basis ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Glucose And Lipid Metabolism ◽  
Care Guidelines

Fibroblast growth factor 21 (FGF21) is a potent endocrine regulator with physiological effects on glucose and lipid metabolism and thus garners much attention for its translational potential for the management of obesity and related metabolic syndromes. FGF21 is mainly expressed in several metabolically active tissue organs, such as the liver, adipose tissue, skeletal muscle, and pancreas, with profound effects and therapeutic relevance. Emerging experimental and clinical data point to the demonstrated metabolic benefits of FGF21, which include, but are not limited to, weight loss, glucose and lipid metabolism, and insulin sensitivity. In addition, FGF21 also acts directly through its coreceptor β-klotho in the brain to alter light-dark cycle activity. In this review, we critically appraise current advances in understanding the physiological actions of FGF21 and its role as a biomarker of various metabolic diseases, especially type 2 diabetes mellitus. We also discuss the potentially exciting role of FGF21 in improving our health and prolonging our life span. This information will provide a fuller understanding for further research into FGF21, as well as providing a scientific basis for potentially establishing health care guidelines for this promising molecule.

scholarly journals Kale supplementation during high fat feeding improves metabolic health in a mouse model of obesity and insulin resistance

PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0256348
Author(s):  
Samnhita Raychaudhuri ◽  
Si Fan ◽  
Olivia Kraus ◽  
Md. Shahinozzaman ◽  
Diana N. Obanda
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Cardiovascular Health ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Fat ◽  
Serum Triglycerides ◽  
Markers Of Inflammation

Cruciferous vegetables have been widely studied for cancer prevention and cardiovascular health. Broccoli is the cruciferous vegetable whose phytochemistry and physiological effects have been most extensively studied. Kale (Brassica oleracea var. acephala) appears on lists of ‘healthiest, nutrient dense foods’ but, there is paucity of data on kale as a functional food. In a 12-week study, we tested the effect of curly green kale on high fat diet (HFD) induced obesity and insulin resistance, lipid metabolism, endotoxemia and inflammation in C57BL/6J mice fed isocaloric diets. Kale supplementation did not attenuate HFD diet induced fat accumulation and insulin resistance (P = ns; n = 9) but, it lowered serum triglycerides, low density lipoprotein (LPL) cholesterol and prevented HFD induced increases in systemic endotoxemia and inflammation (serum LPS and Ccl2) (P<0.01; n = 9). In adipose tissue, kale enhanced the expression of genes involved in adipogenesis (P<0.01; n = 9), reduced the appearance of histologic markers of inflammation, downregulated both the gene expression and protein expression of the adipose tissue specific inflammation markers CD11c and F4/80 (P<0.001; n = 9) and reduced the gene expression of a battery of chemokine C-C motif ligands (Ccl2, Ccl6, Ccl7, Ccl8, Ccl9) and chemokine C-C motif receptors (Ccr2, Ccr3, Ccr5). We conclude that kale vegetable protects against HFD diet induced dysfunction through mechanisms involving lipid metabolism, endotoxemia and inflammation.

Glucose and lipid metabolism alterations in liver and adipose tissue pre-dispose p47phox knockout mice to systemic insulin resistance

2018 ◽  
Vol 52 (5) ◽  
pp. 568-582 ◽  
Author(s):  
Babu Nageswararao Kanuri ◽  
Sanjay C. Rebello ◽  
Priya Pathak ◽  
Hobby Agarwal ◽  
Jitendra S. Kanshana ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Knockout Mice ◽  
Glucose And Lipid Metabolism ◽  
Systemic Insulin Resistance

scholarly journals Insights into the role of macrophage migration inhibitory factor in obesity and insulin resistance

2012 ◽  
Vol 71 (4) ◽  
pp. 622-633 ◽  
Author(s):  
Orla M. Finucane ◽  
Clare M. Reynolds ◽  
Fiona C. McGillicuddy ◽  
Helen M. Roche
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Metabolic Diseases ◽  
Inhibitory Factor ◽  
Low Grade ◽  
Macrophage Migration ◽  
Pharmacological Agents

High-fat diet (HFD)-induced obesity has emerged as a state of chronic low-grade inflammation characterised by a progressive infiltration of immune cells, particularly macrophages, into obese adipose tissue. Adipose tissue macrophages (ATM) present immense plasticity. In early obesity, M2 anti-inflammatory macrophages acquire an M1 pro-inflammatory phenotype. Pro-inflammatory cytokines including TNF-α, IL-6 and IL-1β produced by M1 ATM exacerbate local inflammation promoting insulin resistance (IR), which consequently, can lead to type-2 diabetes mellitus (T2DM). However, the triggers responsible for ATM recruitment and activation are not fully understood. Adipose tissue-derived chemokines are significant players in driving ATM recruitment during obesity. Macrophage migration inhibitory factor (MIF), a chemokine-like inflammatory regulator, is enhanced during obesity and is directly associated with the degree of peripheral IR. This review focuses on the functional role of macrophages in obesity-induced IR and highlights the importance of the unique inflammatory cytokine MIF in propagating obesity-induced inflammation and IR. Given MIF chemotactic properties, MIF may be a primary candidate promoting ATM recruitment during obesity. Manipulating MIF inflammatory activities in obesity, using pharmacological agents or functional foods, may be therapeutically beneficial for the treatment and prevention of obesity-related metabolic diseases.

scholarly journals FGF21 as an Endocrine Regulator in Lipid Metabolism: From Molecular Evolution to Physiology and Pathophysiology

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Yusuke Murata ◽  
Morichika Konishi ◽  
Nobuyuki Itoh
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Molecular Evolution ◽  
Ketogenic Diet ◽  
Metabolic Diseases ◽  
Cultured Cells ◽  
Pharmacological Effects ◽  
Glucose And Lipid Metabolism ◽  
Physiological Regulator ◽  
Related Proteins

The FGF family comprises twenty-two structurally related proteins with functions in development and metabolism. TheFgf21gene was generated early in vertebrate evolution. FGF21 acts as an endocrine regulator in lipid metabolism. HepaticFgf21expression is markedly induced in mice by fasting or a ketogenic diet. Experiments withFgf21transgenic mice and cultured cells indicate that FGF21 exerts pharmacological effects on glucose and lipid metabolism in hepatocytes and adipocytes via cell surface FGF receptors. However, experiments withFgf21knockout mice indicate that FGF21 inhibits lipolysis in adipocytes during fasting and attenuates torpor induced by a ketogenic diet but maybe not a physiological regulator for these hepatic functions. These findings suggest the pharmacological effects to be distinct from the physiological roles. Serum FGF21 levels are increased in patients with metabolic diseases having insulin resistance, indicating that FGF21 is a metabolic regulator and a biomarker for these diseases.

scholarly journals Removal of Epididymal Visceral Adipose Tissue Prevents Obesity-Induced Multi-organ Insulin Resistance in Male Mice

2021 ◽  
Vol 5 (5) ◽  
Author(s):  
Michael P Franczyk ◽  
Mai He ◽  
Jun Yoshino
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Visceral Adipose Tissue ◽  
Body Weight Gain ◽  
Whole Body ◽  
Atherogenic Dyslipidemia ◽  
Glucose And Lipid Metabolism ◽  
Visceral Adipose

Abstract Obesity is associated with insulin resistance, an important risk factor of type 2 diabetes, atherogenic dyslipidemia, and nonalcoholic fatty liver disease. The major purpose of this study was to test hypothesize that prophylactic removal of epididymal visceral adipose tissue (VAT) prevents obesity-induced multi-organ (liver, skeletal muscle, adipose tissue) insulin resistance. Accordingly, we surgically removed epididymal VAT pads from adult C57BL/6J mice and evaluated in vivo and cellular metabolic pathways involved in glucose and lipid metabolism following chronic high-fat diet (HFD) feeding. We found that VAT removal decreases HFD-induced body weight gain while increasing subcutaneous adipose tissue (SAT) mass. Strikingly, VAT removal prevents obesity-induced insulin resistance and hyperinsulinemia and markedly enhances insulin-stimulated AKT-phosphorylation at serine-473 (Ser473) and threonine-308 (Thr308) sites in SAT, liver, and skeletal muscle. VAT removal leads to decreases in plasma lipid concentrations and hepatic triglyceride (TG) content. In addition, VAT removal increases circulating adiponectin, a key insulin-sensitizing adipokine, whereas it decreases circulating interleukin 6, a pro-inflammatory adipokine. Consistent with these findings, VAT removal increases adenosine monophosphate–activated protein kinase C phosphorylation, a major downstream target of adiponectin signaling. Data obtained from RNA sequencing suggest that VAT removal prevents obesity-induced oxidative stress and inflammation in liver and SAT, respectively. Taken together, these findings highlight the metabolic benefits and possible action mechanisms of prophylactic VAT removal on obesity-induced insulin resistance and hepatosteatosis. Our results also provide important insight into understanding the extraordinary capability of adipose tissue to influence whole-body glucose and lipid metabolism as an active endocrine organ.

scholarly journals Hepatic insulin resistance and increased hepatic glucose production in mice lacking Fgf21

2015 ◽  
Vol 226 (3) ◽  
pp. 207-217 ◽  
Author(s):  
João Paulo G Camporez ◽  
Mohamed Asrih ◽  
Dongyan Zhang ◽  
Mario Kahn ◽  
Varman T Samuel ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Insulin Resistance ◽  
Whole Body ◽  
Fibroblast Growth Factor 21 ◽  
Glucose And Lipid Metabolism ◽  
Hepatic Glucose

Fibroblast growth factor 21 (FGF21) is an important regulator of hepatic glucose and lipid metabolism and represents a potential pharmacological agent for the treatment of type 2 diabetes and obesity. Mice fed a ketogenic diet (KD) develop hepatic insulin resistance in association with high levels of FGF21, suggesting a state of FGF21 resistance. To address the role of FGF21 in hepatic insulin resistance, we assessed insulin action in FGF21 whole-body knock-out (FGF21 KO) male mice and their littermate WT controls fed a KD. Here, we report that FGF21 KO mice have hepatic insulin resistance and increased hepatic glucose production associated with an increase in plasma glucagon levels. FGF21 KO mice are also hypometabolic and display increased fat mass compared with their WT littermates. Taken together, these findings support a major role of FGF21 in regulating energy expenditure and hepatic glucose and lipid metabolism, and its potential role as a candidate in the treatment of diseases associated with insulin resistance.

Role of Adipokines in Obesity and Obesity related Metabolic Disorders

2021 ◽  
pp. 4261-4264
Author(s):  
Jayamathi Govindaraj ◽  
Keerthidaa Govindaraj ◽  
S. Raghavendra Jayesh ◽  
Kesavaram Padmavathy ◽  
Mathangi Ramalingam ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Cardiovascular Risk ◽  
Metabolic Disorders ◽  
Vital Role ◽  
Novel Therapies ◽  
Metabolic Homeostasis ◽  
Associated Diseases

Obesity is defined as an excessive growth of adipose tissue. It is associated with over nutrition, which impairs systemic metabolic homeostasis. Adipokines secreted by adipose tissue could play an vital role in the development of obesity and associated metabolic disorders includes insulin resistance, inflammation, hypertension, cardiovascular risk etc. Adipokines will be of importance in the development of novel therapies for obesity-associated diseases. This review emphasises on obesity and the role of some Adipokines in obesity and related metabolic disorders.

Current understanding of the role of microRNAs from adipose-derived extracellular vesicles in obesity

2021 ◽  
Author(s):  
Le Zhao ◽  
Haili Yang ◽  
Xingchun Li ◽  
Yongju Zhao
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Extracellular Vesicles ◽  
Metabolic Diseases ◽  
Health Concern ◽  
Regulatory Processes ◽  
Wide Range ◽  
New Research ◽  
Regulatory Functions

Obesity and its associated metabolic diseases, including diabetes, insulin resistance, and inflammation, are rapidly becoming a global health concern. Moreover, obese individuals are more likely to be infected with COVID-19. New research on adipose tissue is required to help us understand these metabolic diseases and their regulatory processes. Recently, extracellular vesicles (EVs) have been identified as novel intercellular vectors with a wide range of regulatory functions. The miRNAs carried by EVs participate in the regulation of white adipose tissue (WAT) browning, insulin resistance, diabetes, and inflammation. In addition, EV miRNAs demonstrate great potential for helping elucidating the mechanism of metabolic diseases, and for advancing their prevention and treatment. In this review, we focus on the mechanisms underlying the regulation of adipose differentiation and metabolic diseases by adipose-derived EV miRNAs. Understanding the role of these miRNAs should enrich our understanding of the etiology and pathogenesis of metabolic diseases caused by obesity.

Sign in / Sign up

Export Citation Format

Share Document