scispace - formally typeset
Open AccessJournal ArticleDOI

Adiponectin, driver or passenger on the road to insulin sensitivity?

Reads0
Chats0
TLDR
Recent findings in the field are summarized and the rodent studies that suggest a causal relationship between adiponectin levels in plasma and systemic insulin sensitivity in perspective are brought in perspective with the currently available data on the clinical side.
Abstract
Almost 20 years have passed since the first laboratory evidence emerged that an abundant message encoding a protein with homology to the C1q superfamily is highly specifically expressed in adipocytes. At this stage, we refer to this protein as adiponectin. Despite more than 10,000 reports in the literature since its initial description, we seem to have written only the first chapter in the textbook on adiponectin physiology. With every new aspect we learn about adiponectin, a host of new questions arise with respect to the underlying molecular mechanisms. Here, we aim to summarize recent findings in the field and bring the rodent studies that suggest a causal relationship between adiponectin levels in plasma and systemic insulin sensitivity in perspective with the currently available data on the clinical side.

read more

Citations
More filters
Journal ArticleDOI

Mechanisms of Insulin Action and Insulin Resistance

TL;DR: This work aims to develop an integrated physiological perspective, placing the intricate signaling effectors that carry out the cell-autonomous response to insulin in the context of the tissue-specific functions that generate the coordinated organismal response.
Journal ArticleDOI

Adipokines in health and disease

TL;DR: Secretion of adipokines, including leptin, adiponectin, fibroblast growth factor 21, retinol-binding protein 4 (RBP4), dipeptidyl peptidase 4 (DPP-4), bone morphogenetic protein (BMP)-4, BMP-7, vaspin, apelin, and progranulin, is altered in adipose tissue dysfunction and may contribute to a spectrum of obesity-associated diseases.
Journal ArticleDOI

Obesity, Oxidative Stress, Adipose Tissue Dysfunction, and the Associated Health Risks: Causes and Therapeutic Strategies.

TL;DR: The role of oxidative stress in the pathogenesis of obesity and its associated risk factors, the role of dysfunctional adipose tissue in development of these risk Factors, and potential strategies to regulate body weight loss/gain for better health benefits are highlighted.
Journal ArticleDOI

Targeting adipose tissue in the treatment of obesity-associated diabetes

TL;DR: An overview of the role of adipose tissue in metabolic homeostasis is provided and emerging novel therapeutic strategies targeting adipOSE tissue are assessed, including adipokine-based strategies, promotion of white adiposa tissue beiging as well as reduction of inflammation and fibrosis.
Journal ArticleDOI

New insight into adiponectin role in obesity and obesity-related diseases.

TL;DR: Adiponectin, exhibiting antihyperglycemic, antiatherogenic, and anti-inflammatory properties, could have important clinical benefits in terms of development of therapies for the prevention and/or for the treatment of obesity and obesity-related diseases.
References
More filters
Book

Molecular Cell Biology

TL;DR: Molecular cell biology, Molecular cell biology , مرکز فناوری اطلاعات و اصاع رسانی, کδاوρزی
Journal ArticleDOI

Adiponectin stimulates glucose utilization and fatty-acid oxidation by activating AMP-activated protein kinase

TL;DR: It is shown that phosphorylation and activation of the 5′-AMP-activated protein kinase (AMPK) are stimulated with globular and full-length Ad in skeletal muscle and only with full- lengths Ad in the liver, indicating that stimulation of glucose utilization and fatty-acid oxidation by Ad occurs through activation of AMPK.
Journal ArticleDOI

The interaction of TIGIT with PVR and PVRL2 inhibits human NK cell cytotoxicity

TL;DR: It is shown that TIGIT is expressed by all human NK cells, that it binds PVR and PVRL2 but not PVRL3 and that it inhibits NK cytotoxicity directly through its ITIM, providing an “alternative self” mechanism for MHC class I inhibition.
Related Papers (5)