Effects of Troglitazone: A new hypoglycemic agent in patients with NIDDM poorly controlled by diet therapy

Iwamoto, Yasuhiko; Kosáka, Kinori; Kuzuya, Tsunehiko; Akanuma, Yasuo; Shigeta, Yukio; Kaneko, Toshio

doi:10.2337/diacare.19.2.151

Cited by 165 publications

(63 citation statements)

References 7 publications

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“…Meanwhile, many researchers have tried to standardize the criteria for defining the responders to TZD treatment with changing FPG or HbA 1c , and thus, the response rates of TZDs have been diversely reported [8,22]. However, since there are no standard cut-off criteria to define the responders to rosiglitazone treatment and for relatively short duration of our trial had been, we classified responders according to the criteria used by Iwamoto et al [8], and found a higher response rate, i.e., 75%.…”

Section: Discussionmentioning

confidence: 99%

“…The thiazolidinedione (TZD) class of antidiabetic agents, such as rosiglitazone and pioglitazone, exert their insulin sensitizing effects on the peroxisome proliferators activated receptor (PPAR)␥ found in insulin-sensitive tissues such as adipose tissue, skeletal muscle, and liver [7][8][9][10][11]. Therefore, the glucose-lowering effects of the TZDs can be distinguished from the sulfonylureas, which act mainly by augmenting insulin secretion, and from the biguanides, which decrease gluconeogenesis and increase peripheral glucose utilization, requiring endogenous insulin to exert their effects.…”

Section: Introductionmentioning

confidence: 99%

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Predictive clinical parameters for therapeutic efficacy of rosiglitazone in Korean type 2 diabetes mellitus

Kim

Soo

Kim

et al. 2005

Diabetes Research and Clinical Practice

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Predictive clinical parameters for therapeutic efficacy of rosiglitazone in Korean type 2 diabetes mellitus

Kim

Soo

Kim

et al. 2005

Diabetes Research and Clinical Practice

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“…Upon ligand binding, PPARs form heterodimers with retinoid X receptor (RXR) and then bind to PPAR-responsive elements in the regulatory region of target genes. Thiazolidinediones (TZDs) are a group of PPARG agonists that are widely used in the treatment of type 2 diabetes [18,19]. Rosiglitazone, a representative TZD, is active in vivo as an anti-diabetic agent in the ob/ob mouse model, and has been used as an oral hypoglycaemic agent in the treatment of type 2 diabetes in humans for many years [20].…”

Section: Introductionmentioning

confidence: 99%

Regulation of adiponectin receptors in hepatocytes by the peroxisome proliferator-activated receptor-γ agonist rosiglitazone

et al. 2006

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Aims/hypothesis: Adiponectin is an adipocytederived hormone that plays a critical role in the development of type 2 diabetes via interaction with adiponectin receptors 1 (ADIPOR1) and 2 (ADIPOR2). Rosiglitazone is a peroxisome proliferator-activated receptor-γ (PPARG) agonist that is widely used in the treatment of type 2 diabetes. We hypothesised that rosiglitazone regulates lipid and glucose metabolism through modulation of the expression of adiponectin receptors in the liver. Methods: The expression of ADIPOR1 and ADIPOR2 was analysed in HepG2 hepatocytes. The promoters of adiponectin receptors were isolated and used to analyse the transcriptional regulation. The expression of adiponectin receptors in the liver was determined in mice treated with rosiglitazone. Results: Rosiglitazone elevated the mRNA and protein levels of ADIPOR2 and stimulated ADIPOR2 promoter in HepG2 cells. Analysis with the ADIPOR2 promoter revealed a putative rosiglitazone-responsive region that contained a glucocorticoid receptor (GR)-binding element. The GR agonist dexamethasone synergised with rosiglitazone to stimulate the ADIPOR2 promoter wheras the GR antagonist RU486 abolished this stimulation. Treatment of mice with rosiglitazone elevated the expression of ADIPOR2 in the liver. Conclusions/interpretation: This study indicates that rosiglitazone can elevate the expression of ADIPOR2 in hepatocytes. Our data also suggest that the PPARG agonist rosiglitazone can interact functionally with a GR element in the ADIPOR2 promoter to mediate stimulation of transcription. This study thus reveals a new paradigm underlying the therapeutic effect of PPARG activators in the treatment of type 2 diabetes.

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“…As in the animal studies, higher baseline BMI and the extent of hypertriglyceridemia predict a better improvement in HbA1c during Troglitazone treatment. 104 Also, the amount of subcutaneous fat and a gender effect (female better than male) have been shown to correlate positively with the TZD-induced improvement in HbA1c. 96,105 Hence, higher baseline BMI is likely to predict a higher weight gain during treatment.…”

Section: Ppargamma Agonistsfadipogenic Treatment Of Type II Diabetes mentioning

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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Effects of Troglitazone: A new hypoglycemic agent in patients with NIDDM poorly controlled by diet therapy

Abstract: Troglitazone at 400 mg/day decreased FPG and HbA1c significantly in NIDDM patients who had failed to respond to diet therapy. Troglitazone, developed as a drug to enhance insulin action, can be a useful hypoglycemic agent for the treatment of NIDDM.

Cited by 165 publications

References 7 publications

Predictive clinical parameters for therapeutic efficacy of rosiglitazone in Korean type 2 diabetes mellitus

Predictive clinical parameters for therapeutic efficacy of rosiglitazone in Korean type 2 diabetes mellitus

Regulation of adiponectin receptors in hepatocytes by the peroxisome proliferator-activated receptor-γ agonist rosiglitazone

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

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