Share This Author
Cloning of adiponectin receptors that mediate antidiabetic metabolic effects
The cloning of complementary DNAs encoding adiponectin receptors 1 and 2 by expression cloning supports the conclusion that they serve as receptors for globular and full-length adiponECTin, and that they mediate increased AMP kinase and PPAR-α ligand activities, as well as fatty-acid oxidation and glucose uptake by adiponectionin.
Adiponectin stimulates glucose utilization and fatty-acid oxidation by activating AMP-activated protein kinase
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.
Adiponectin and adiponectin receptors.
It is shown that AdipoR1 and AdIPoR2 serve as receptors for globular and full-length adiponectin and mediate increased AMP-activated protein kinase, peroxisome proliferator-activated receptor-alpha ligand activities, and glucose uptake and fatty-acid oxidation by adiponECTin.
The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity
It is concluded that decreased adiponectin is implicated in the development of insulin resistance in mouse models of both obesity and lipoatrophy and that the replenishment of adiponECTin might provide a novel treatment modality for insulin resistance and type 2 diabetes.
CD8+ effector T cells contribute to macrophage recruitment and adipose tissue inflammation in obesity
The findings suggest that obese adipose tissue activates CD8+ T cells, which, in turn, promote the recruitment and activation of macrophages in this tissue, which supports the notion that CD8- T cells have an essential role in the initiation and propagation of adipose inflammation.
Adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome.
- T. Kadowaki, T. Yamauchi, N. Kubota, K. Hara, K. Ueki, K. Tobe
- Medicine, BiologyThe Journal of clinical investigation
- 3 July 2006
The pathophysiology of adiponectin and adiponECTin receptors in insulin resistance, diabetes, and the metabolic syndrome is described and potential versatile therapeutic targets to combat obesity-linked diseases characterized by insulin resistance are described.
Diabetes in Asia: epidemiology, risk factors, and pathophysiology.
Type 2 diabetes is an increasing epidemic in Asia, characterized by rapid rates of increase over short periods and onset at a relatively young age and low body mass index; prevention and control of diabetes should be a top public health priority in Asian populations.
Targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and metabolic actions
Adenovirus-mediated expression of AdipoR1 and R2 in the liver of Lepr−/− mice increased AMP-activated protein kinase (AMPK) activation and peroxisome proliferator-activated receptor (PPAR)-α signaling pathways, respectively, and abolished adiponectin binding and actions, leading to insulin resistance and marked glucose intolerance in vivo.
Report of the Committee on the Classification and Diagnostic Criteria of Diabetes Mellitus
Diabetes mellitus is a group of diseases associated with various metabolic disorders, the main feature of which is chronic hyperglycemia due to insufficient insulin action, which can cause susceptibility to specific complications and also foster arteriosclerosis.
Variants in KCNQ1 are associated with susceptibility to type 2 diabetes mellitus
The data implicate KCNQ1 as a diabetes susceptibility gene in groups of different ancestries as well as in two independent Japanese populations, and the risk allele of this polymorphism was associated with impairment of insulin secretion according to the homeostasis model assessment of β-cell function or the corrected insulin response.