More than a simple storage organ: Adipose tissue as a source of adipokines involved in cardiovascular disease

2013 ◽  
Vol 110 (10) ◽  
pp. 641-650 ◽  
Author(s):  
Gersina Rega-Kaun ◽  
Christoph Kaun ◽  
Johann Wojta
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Overweight And Obesity ◽  
Therapeutic Approaches ◽  
Storage Organ ◽  
Pathophysiological Role ◽  
Metabolically Healthy

SummaryOverweight and obesity in many countries have developed into a serious health problem by themselves and by their impact on other pathologies such as insulin resistance, type 2 diabetes, hypertension, heart disease and cancer. The modulation of these diseases by adipose tissue-derived biomolecules, so-called adipokines, could be the key to differentiate between metabolically healthy and unhealthy obesity. This review will discuss the pathophysiological role of selected adipokines, primarily focusing on cardiovascular diseases. Furthermore, we will highlight possible therapeutic approaches, which target these biomolecules.

scholarly journals Potential Roles of Adipocyte Extracellular Vesicle–Derived miRNAs in Obesity-Mediated Insulin Resistance

2020 ◽  
Author(s):  
Yujeong Kim ◽  
Ok-Kyung Kim
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Metabolic Disorders ◽  
Extracellular Vesicle ◽  
Extracellular Mirnas

ABSTRACT Recently, extracellular microRNAs (miRNAs) from adipose tissue have been shown to be involved in the development of insulin resistance. Here, we summarize several mechanisms explaining the pathogenesis of obesity-induced insulin resistance and associated changes in the expression of obesity-associated extracellular miRNAs. We discuss how miRNAs, particularly miR-27a, miR-34a, miR-141-3p, miR-155, miR210, and miR-222, in extracellular vesicles secreted from the adipose tissue can affect the insulin signaling pathway in metabolic tissue. Understanding the role of these miRNAs will further support the development of therapeutics for obesity and metabolic disorders such as type 2 diabetes.

scholarly journals An Update to the WISP-1/CCN4 Role in Obesity, Insulin Resistance and Diabetes

Medicina ◽  
2021 ◽  
Vol 57 (2) ◽  
pp. 100
Author(s):  
Małgorzata Mirr ◽  
Maciej Owecki
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Energy Homeostasis ◽  
Peripheral Tissues ◽  
Insulin Resistant ◽  
Highly Active ◽  
Underlying Processes

Insulin resistance refers to the diminished response of peripheral tissues to insulin and is considered the major risk factor for type 2 diabetes. Although many possible mechanisms have been reported to develop insulin resistance, the exact underlying processes remain unclear. In recent years, the role of adipose tissue as a highly active metabolic and endocrine organ, producing proteins called adipokines and their multidirectional activities has gained interest. The physiological effects of adipokines include energy homeostasis and insulin sensitivity regulation. In addition, an excess of adipose tissue is followed by proinflammatory state which results in dysregulation of secreted cytokines contributing to insulin resistance. Wingless-type (Wnt) inducible signalling pathway protein-1 (WISP-1), also known as CCN4, has recently been described as a novel adipokine, whose circulating levels are elevated in obese and insulin resistant individuals. Growing evidence suggests that WISP-1 may participate in the impaired glucose homeostasis. In this review, we characterize WISP-1 and summarize the latest reports on the role of WISP-1 in obesity, insulin resistance and type 2 diabetes.

scholarly journals RGC32 deficiency protects against high-fat diet-induced obesity and insulin resistance in mice

2014 ◽  
Vol 224 (2) ◽  
pp. 127-137 ◽  
Author(s):  
Xiao-Bing Cui ◽  
Jun-Na Luan ◽  
Jianping Ye ◽  
Shi-You Chen
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Tolerance Test ◽  
High Fat ◽  
Diet Induced Obesity

Obesity is an important independent risk factor for type 2 diabetes, cardiovascular diseases and many other chronic diseases. Adipose tissue inflammation is a critical link between obesity and insulin resistance and type 2 diabetes and a contributor to disease susceptibility and progression. The objective of this study was to determine the role of response gene to complement 32 (RGC32) in the development of obesity and insulin resistance. WT and RGC32 knockout (Rgc32−/− (Rgcc)) mice were fed normal chow or high-fat diet (HFD) for 12 weeks. Metabolic, biochemical, and histologic analyses were performed. 3T3-L1 preadipocytes were used to study the role of RGC32 in adipocytes in vitro. Rgc32−/− mice fed with HFD exhibited a lean phenotype with reduced epididymal fat weight compared with WT controls. Blood biochemical analysis and insulin tolerance test showed that RGC32 deficiency improved HFD-induced dyslipidemia and insulin resistance. Although it had no effect on adipocyte differentiation, RGC32 deficiency ameliorated adipose tissue and systemic inflammation. Moreover, Rgc32−/− induced browning of adipose tissues and increased energy expenditure. Our data indicated that RGC32 plays an important role in diet-induced obesity and insulin resistance, and thus it may serve as a potential novel drug target for developing therapeutics to treat obesity and metabolic disorders.

scholarly journals Bisphenols and the Development of Type 2 Diabetes: The Role of the Skeletal Muscle and Adipose Tissue

Environments ◽  
2021 ◽  
Vol 8 (4) ◽  
pp. 35
Author(s):  
Fozia Ahmed ◽  
Maria João Pereira ◽  
Céline Aguer
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Bisphenol A ◽  
Cross Talk ◽  
Environmental Contaminants ◽  
Bisphenol S

Bisphenol A (BPA) and bisphenol S (BPS) are environmental contaminants that have been associated with the development of insulin resistance and type 2 diabetes (T2D). Two organs that are often implicated in the development of insulin resistance are the skeletal muscle and the adipose tissue, however, seldom studies have investigated the effects of bisphenols on their metabolism. In this review we discuss metabolic perturbations that occur in both the skeletal muscle and adipose tissue affected with insulin resistance, and how exposure to BPA or BPS has been linked to these changes. Furthermore, we highlight the possible effects of BPA on the cross-talk between the skeletal muscle and adipose tissue.

Review: Obesity Induced Insulin Resistance, Type 2 Diabetes and Emerging Therapeutic Approaches.

2021 ◽  
pp. 1-22
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Type 2 Diabetes Mellitus ◽  
Adipose Tissue ◽  
Obese Patients ◽  
Therapeutic Approaches ◽  
Tnf Α

There is a strong association between obesity, insulin resistance and type 2 diabetes mellitus. Abdominal obesity appears to be a major mediator of insulin resistance and hyperinsulinemia. Insulin resistance is a pathological condition in which cells fail to respond normally to the hormone insulin. leading to high blood sugar (impaired glucose uptake in peripheral tissues, particularly in skeletal muscle.) The more life-threatening problems fall into four main areas: type 2 diabetes, cardiovascular diseases (CVD), dyslipidemia and certain types of cancers and musculoskeletal disorders. There is considerable evidence that inflammation is a primary mediator of obesity induced insulin resistance and related co-morbidities, including diabetes and CVD whereby pro-inflammatory substances and other chemokines produced by adipocytes and macrophages are able to cause insulin resistance. The major inflammatory factors include pro-inflammatory interleukins (IL-1 & IL-6) and signaling intermediate-nuclear factor kappa B cells (NF-kB), chemokines and cytokines, tumor necrosis factor alpha (TNF-α), adiponectin (ADN), circulating C-reactive protein (CRP) concentrations, toll-like receptors (Tlr), free fatty acids (FFA), oxidative stress and dietary fatty acids. Considering this viewpoint, in the present review, we have selected ten well designed clinical studies with salsalates, thiazolidinediones (TZD) and TNF-α–antagonists to discuss and analyze these emerging therapeutic approaches for the treatment of obesity induced insulin resistance and type 2 diabetes mellitus. These therapeutics provide sufficient evidence of improved glycemic control post treatment in obese patients by targeting the state of chronic inflammation that characterizes obesity and resulted in improved insulin sensitivity by reducing adipocyte pro-inflammatory cytokine expression, adipose tissue macrophage content and immune cell infiltration into adipose tissue and other inflammatory markers. Even with looking at only few studies, analyzing each pathway, the hypothesis that targeting pro-inflammatory pathways in adipocytes with TZD and salicylates as a novel approach remains supported for reducing chronic inflammation-induced insulin resistance in obese patients, with TZD emerging with the strongest effects.

scholarly journals Brd2 disruption in mice causes severe obesity without Type 2 diabetes

2009 ◽  
Vol 425 (1) ◽  
pp. 71-85 ◽  
Author(s):  
Fangnian Wang ◽  
Hongsheng Liu ◽  
Wanda P. Blanton ◽  
Anna Belkina ◽  
Nathan K. Lebrasseur ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Glucose Intolerance ◽  
Severe Obesity ◽  
Healthy Humans ◽  
Brown Adipose ◽  
Metabolically Healthy

Certain human subpopulations are metabolically healthy but obese, or metabolically obese but normal weight; such mutations uncouple obesity from glucose intolerance, revealing pathways implicated in Type 2 diabetes. Current searches for relevant genes consume significant effort. We have reported previously a novel double bromodomain protein called Brd2, which is a transcriptional co-activator/co-repressor with SWI/SNF (switch mating type/sucrose non-fermenting)-like functions that regulates chromatin. In the present study, we show that wholebody disruption of Brd2, an unusual MHC gene, causes lifelong severe obesity in mice with pancreatic islet expansion, hyperinsulinaemia, hepatosteatosis and elevated pro-inflammatory cytokines, but, surprisingly, enhanced glucose tolerance, elevated adiponectin, increased weight of brown adipose tissue, heat production and expression of mitochondrial uncoupling proteins in brown adipose tissue, reduced macrophage infiltration in white adipose tissue, and lowered blood glucose, leading to an improved metabolic profile and avoiding eventual Type 2 diabetes. Brd2 is highly expressed in pancreatic β-cells, where it normally inhibits β-cell mitosis and insulin transcription. In 3T3-L1 pre-adipocytes, Brd2 normally co-represses PPAR-γ (peroxisome-proliferator-activated receptor-γ) and inhibits adipogenesis. Brd2 knockdown protects 3T3-L1 adipocytes from TNF-α (tumour necrosis factor-α)-induced insulin resistance, thereby decoupling inflammation from insulin resistance. Thus hypomorphic Brd2 shifts energy balance toward storage without causing glucose intolerance and may provide a novel model for obese metabolically healthy humans.

scholarly journals The Association between Monocyte Surface CD163 and Insulin Resistance in Patients with Type 2 Diabetes

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Reina Kawarabayashi ◽  
Koka Motoyama ◽  
Miyuki Nakamura ◽  
Yuko Yamazaki ◽  
Tomoaki Morioka ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Model Assessment ◽  
Fluorescent Intensity ◽  
Expression Levels ◽  
Cd163 Expression ◽  
Pathophysiological Role ◽  
Simple Regression Analysis

Aim. To investigate the association between monocyte CD163 and insulin resistance in patients with type 2 diabetes.Methods. One hundred sixty-six patients with type 2 diabetes without inflammatory or chronic kidney disease were recruited. The monocyte CD163 levels were measured by flow cytometry and soluble CD163 (sCD163) by ELISA. Insulin resistance was evaluated by the index of the homeostasis model assessment (HOMA-R).Results. The median sCD163 and monocyte CD163 expression levels were 582.9 (472.4–720.0) ng/ml and 6061 (4486–7876) mean fluorescent intensity (MFI), respectively. In a simple regression analysis, monocyte CD163 was inversely correlated with log [HOMA-R] (r=–0.257,p=0.010), and sCD163 was positively correlated with log [HOMA-R] (r=0.198,p=0.042). In multiple regression analyses, monocyte CD163 was an independent contributor to log [HOMA-R] (β=–0.220,p=0.020) even after adjustment of various clinical factors for HOMA-R (R2=0.281,p=0.001), whereas sCD163 was not.Conclusions. Monocyte surface CD163 expression levels were more significantly associated with insulin resistance than sCD163 in patients with type 2 diabetes, suggesting a novel pathophysiological role of CD163.

1758-P: Type 2 Diabetes–Associated Mood Disorders: Role of Insulin Resistance in Serotonergic Neurons

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1758-P
Author(s):  
HUGO MARTIN ◽  
SÉBASTIEN BULLICH ◽  
FABIEN DUCROCQ ◽  
MARION GRALAND ◽  
CLARA OLIVRY ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Mood Disorders ◽  
Serotonergic Neurons ◽  
P Type
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