Role of PPARγ, transcriptional cofactors, and adiponectin in the regulation of nutrient metabolism, adipogenesis and insulin action: view from the chair

2005 ◽  
Vol 29 (S1) ◽  
pp. S3-S4 ◽  
Author(s):  
J P Berger
1994 ◽  
Vol 22 (2) ◽  
pp. 516-522 ◽  
Author(s):  
Loranne Agius ◽  
Matthew Peak ◽  
Guy Beresford ◽  
Molham Al-Habori ◽  
Trevor H. Thomas

1987 ◽  
Vol 242 (3) ◽  
pp. 655-660 ◽  
Author(s):  
M J Fisher ◽  
A J Dickson ◽  
C I Pogson

The stimulation of phenylalanine hydroxylation in isolated liver cells by sub-maximally effective concentrations of glucagon (less than 0.1 microM) is antagonized by insulin (0.1 nM-0.1 microM). This phenomenon is a consequence of a decrease in the glucagon-stimulated phosphorylation of phenylalanine hydroxylase from liver cells incubated in the presence of insulin. The impact of insulin on the phosphorylation state and activity of the hydroxylase is mimicked by incubation of liver cells in the presence of orthovanadate (10 microM). A series of cyclic AMP and cyclic GMP analogues enhanced phenylalanine hydroxylation: in each case insulin diminished the stimulation of flux. These results are discussed in the light of the characteristics of insulin action on other metabolic processes.


1997 ◽  
Vol 9 (1) ◽  
pp. 18-32 ◽  
Author(s):  
Craig A. Horswill ◽  
William B. Zipf ◽  
C. Lawrence Kien ◽  
E. Bowie Kahle

Insulin is an anabolic hormone with stimulatory effects on glucose and amino acid uptake, possibly protein synthesis, and bone growth, and inhibitory effects on protein breakdown. The precise role of insulin in the growth of healthy children is unclear, but two clinical models can be examined to illustrate insulin’s potential role in the growth of children. The cystic fibrosis (CF) patient, who exhibits poor linear growth and low lean body mass, may exhibit inadequate insulin secretion or impaired insulin action. The obese child typically has an excess of peripheral insulin, an associated acceleration of linear growth, and an accretion of lean body mass and adipose tissue. Speculation is offered on the putative role of exercise in affecting insulin action and secretion, which in turn could impact growth in children with CF or obesity.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Zhiyou Zhang ◽  
Hwi Jin Ko ◽  
Dae Young Jung ◽  
Zhexi Ma ◽  
Jason K Kim

Increasing evidence implicates the role of inflammation in the pathogenesis of diabetes and complications. Inflammatory cytokines (IL-6, TNF-α) are elevated in obese diabetic subjects, and are shown to modulate glucose metabolism in peripheral organs. In this report, we examined the effects of IL-6 on cardiac metabolism and insulin action in vivo. Male C57BL/6 mice were intravenously treated with IL-6 (16 ng/hr) or saline (control) for 2 hrs, and [ 14 C]2-deoxyglucose was intravenously injected in awake mice to measure myocardial glucose metabolism (n=9~10). Hyperinsulinemic-euglycemic clamps (2.5 mU/kg/min insulin infusion) were also performed in IL-6 or saline-treated mice (n=4~5) to measure cardiac insulin action. Acute treatment with IL-6 caused a 25% increase in myocardial STAT3 activity and significantly reduced basal myocardial glucose metabolism (Fig. 1 ; * P< 0.05). IL-6 treatment also reduced insulin-stimulated glucose uptake in heart, and these effects were associated with marked decreases in AMPK activity (Thr-phosphorylation of AMPK; Fig. 2 ) and IRS-1 tyrosine phosphorylation (Fig. 3 ). Acute IL-6 treatment increased myocardial expression of PKC-𝛉, which has been shown to mediate insulin resistance in peripheral organs (Fig. 4 ). These results indicate that IL-6 is a potent negative regulator of myocardial glucose metabolism and insulin action, and the underlying mechanism may involve IL-6 mediated activation of PKC-𝛉 and defects in AMPK and insulin signaling activity. Thus, our findings suggest a potential role of IL-6 in the pathogenesis of diabetic heart failure.


1997 ◽  
Vol 16 (1) ◽  
pp. 3-11 ◽  
Author(s):  
J.H. Cummings ◽  
G.T. Macfarlane

Sign in / Sign up

Export Citation Format

Share Document