Skeletal muscle peroxisome proliferator- activated receptor-gamma expression in obesity and non- insulin-dependent diabetes mellitus.

Kruszynska, Yolanta T.; Mukherjee, Ranjan; Jow, Lily; Dana, Sharon L.; Paterniti, James R.; Olefsky, Jerrold M.

doi:10.1172/jci1076

Cited by 89 publications

(66 citation statements)

References 38 publications

(38 reference statements)

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“…In agreement with our previous finding in muscle, a recent report also found PPARg mRNA in adipose tissue to be increased after a 3-h hyperinsulinaemic, euglycaemic clamp [38]. Other investigators found no change in skeletal muscle PPARg1 mRNA after 5 h of hyperinsulinaemia [39]. This discrepancy could also represent a potential transient nature of the insulin effect to increase gene expression, it could have returned to baseline by 5 h. There are other examples of such transient responses in gene expression to insulin exposure [40].…”

Section: Discussionsupporting

confidence: 92%

Distribution of peroxisome proliferator-activated receptors (PPARs) in human skeletal muscle and adipose tissue: relation to insulin action

et al. 2000

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Section: Discussionsupporting

confidence: 92%

Distribution of peroxisome proliferator-activated receptors (PPARs) in human skeletal muscle and adipose tissue: relation to insulin action

et al. 2000

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“…10 On the contrary, other studies found no correlation between subcutaneous or omental adipose tissue PPARg mRNA and BMI. 11,13,46 Also, in Rhesus monkeys there was no correlation between total PPARg adipose tissue mRNA expression and obesity, but the ratio of PPARg2/total PPARg was positively correlated with obesity and fasting insulin concentration. 47 In addition, in obese human subjects, the ratio of PPARg expression in omental/subcutaneous adipose PPARgamma agonistsFadipogenic treatment of type II diabetes TM Larsen et al tissue was increased compared to normal weight subjects, suggesting that the relative PPARg expression is increased in omental fat in obesity.…”

Section: Pparg Activation Induces Transcription Of Genes Involved In mentioning

confidence: 94%

“…10 These results were corroborated in other studies in humans. [11][12][13] In addition to adipose tissue, PPARg is expressed at rather high levels in the large intestine.…”

Section: Introductionmentioning

confidence: 99%

PPARgamma agonists in the treatment of type II diabetes: is increased fatness commensurate with long-term efficacy?

Larsen¹,

Toubro²,

Astrup³

2003

Int J Obes

258

170

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The nuclear hormone receptor peroxisome proliferator-activated receptor gamma (PPARg) is a member of the PPAR family. The endogenous activators of all members of the PPAR family are a variety of fatty acids, which suggests that the PPARs are highly involved in lipid metabolism. In the present paper, the current understanding of the involvement of PPARg in adipocyte proliferation and adipose tissue formation is extensively reviewed, and it is stressed that PPARg seems to be a major regulator in the differentiation of adipocytes. Thiazoledinediones (TZDs) are a group of PPARg-agonists used in the treatment of type 2 diabetes (T2D) since 1997. They are characterized by their ability to decrease insulin resistance, and have been suggested to slow down the progression of insulin resistance. Treatment with TZD requires several weeks of treatment to decrease plasma glucose levels, but in addition they markedly decrease plasma triglycerides and free fatty acids. A major drawback of treatment with TZD is body fat gain, but some evidence suggests that the fat is redistributed in a favourable direction, that is, from visceral to subcutaneous depots. However, the effect of long-term treatment on weight gain following TZD treatment is unknown, and it may be questioned whether the use of these 'adipogenic compounds' is appropriate, considering that excess body fat is almost a prerequisite for the development of type 2 diabetes.

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“…Analytical procedures. Plasma and infusate [ 3 H]glucose specific activity were determined as previously described (34). Insulin was measured by a double-antibody technique (35).…”

Section: Methodsmentioning

confidence: 99%

Effects of troglitazone on blood concentrations of plasminogen activator inhibitor 1 in patients with type 2 diabetes and in lean and obese normal subjects.

et al. 2000

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Low plasma fibrinolytic activity in association with increased plasma plasminogen activator inhibitor 1 ( PAI-1) levels has been linked to an increased risk of atherosclerosis in obesity and type 2 diabetes. We tested the hypothesis that troglitazone, which improves insulin sensitivity and lowers plasma insulin levels in insulin-resistant obese subjects and patients with t y p e 2 diabetes, would also lower circulating PA I -1 antigen concentrations and activity. We assessed insulin sensitivity (5-h, 80 mU · m -2 · min -1 h y p e r i n s ulinemic-euglycemic clamp) and measured plasma PA I -1 antigen and activities and tissue plasminogen activator ( t PA) in 14 patients with type 2 diabetes and 20 normal control subjects (10 lean, 10 obese) before and after 3 months of treatment with troglitazone (600 m g / d a y ) . At baseline, plasma PAI-1 antigen levels after an overnight fast were significantly higher in the obese (33.5 ± 4.7 µg/l) and type 2 diabetic subjects (54.9 ± 6.3 µg/l) than in the lean control subjects (16.3 ± 3.2 µg/l; P < 0.01 and P < 0.001, respectively). Troglitazone decreased plasma PAI-1 antigen concentrations in the diabetic patients (36.8 ± 5.0 µg/l; P < 0.001 vs. baseline), but the reduction in the obese subjects did not reach statistical significance (baseline, 33.5 ± 4.7; after troglitazone, 2 5 . 6 ± 5.2 µg/l). Changes in plasma PAI-1 activity paralleled those of PAI-1 antigen. The extent of the reduction in plasma PAI-1 antigen concentrations in the diabetic patients after troglitazone correlated with the reductions in fasting plasma insulin (r = 0.60, P < 0.05), nonesterified fatty acid (r = 0.63, P < 0.02), and glucose concentrations (r = 0.64, P < 0.02) but not with the improvement in glucose disposal rates during the glucose clamps. Three nonresponders to troglitazone with respect to effects on insulin sensitivity and fasting glucose and insulin levels also had no reduction in circulating PAI-1. In conclusion, troglitazone enhances fibrinolytic system activity in insulin-resistant type 2 diabetic patients. This effect appears to be intimately linked to its potential to lower plasma insulin levels and improve glycemic control through its peripheral tissue insulin-sensitizing effects. Diabetes 4 9 :6 3 3-639, 2000 A ccelerated atherosclerosis is an important cause of morbidity and mortality in insulin-resistant obese subjects and patients with type 2 diabetes (1,2). Low fibrinolytic activity in blood is a wellrecognized major risk factor not only for thrombosis, but also for atherosclerosis (3,4). Deficient fibrinolysis is due primarily to increased concentrations in blood of plasminogen activator inhibitor 1 (PAI-1), which rapidly binds to and inactivates tissue plasminogen activator (tPA) (5). PAI-1 concentrations and activity are increased in obese subjects (6-8) and patients with type 2 diabetes (8-13). The increases may contribute to an excess risk of cardiovascular disease (4,12-14).PAI-1 levels correlate with a number of variables that cosegregate in subjects with the insulin r...

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Skeletal muscle peroxisome proliferator- activated receptor-gamma expression in obesity and non- insulin-dependent diabetes mellitus.

Cited by 89 publications

References 38 publications

Distribution of peroxisome proliferator-activated receptors (PPARs) in human skeletal muscle and adipose tissue: relation to insulin action

Distribution of peroxisome proliferator-activated receptors (PPARs) in human skeletal muscle and adipose tissue: relation to insulin action

PPARgamma agonists in the treatment of type II diabetes: is increased fatness commensurate with long-term efficacy?

Effects of troglitazone on blood concentrations of plasminogen activator inhibitor 1 in patients with type 2 diabetes and in lean and obese normal subjects.

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