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Tetsuro Ishii – One of the best experts on this subject based on the ideXlab platform.

  • the α glucosidase inhibitor Acarbose prevents obesity and simple steatosis in sequestosome 1 a170 p62 deficient mice
    Hepatology Research, 2009
    Co-Authors: Kosuke Okada, Toru Yanagawa, Eiji Warabi, Keiko Yamastu, Junya Uwayama, Koichi Takeda, Hirotoshi Utsunomiya, Hiroshi Yoshida, Junichi Shoda, Tetsuro Ishii

    Abstract:

    Aim Sequestosome 1 (SQSTM1)/A170/p62 plays an important role in membrane-receptor mediated signal transduction and autophagic protein degradation. Although the mechanism involved is not clear, sqstm1 gene knockout (KO) mice develop mature-onset obesity and insulin resistance, leading to type II diabetes. KO mice show accumulation of fat in white adipose tissue and the liver when fed a standard diet. Acarbose is an alpha-glucosidase inhibitor that improves insulin sensitivity and decreases postprandial hyperglycemia, and it is used to treat type 2 diabetes. We examined whether or not dietary Acarbose prevented obesity and simple steatosis in KO mice. Methods Wild-type (WT) and KO mice were fed a standard diet with or without Acarbose (0.8% w/w) from 15-25 weeks of age. The body weight and the fat content of adipose tissue and the liver were measured, and changes of lipid metabolism in these tissues were assessed from gene expression. Results Acarbose treatment suppressed weight gain and the development of hepatic steatosis in KO mice. Acarbose treatment up-regulated hepatic expression of the pparalpha, ucp-2, and abca1 genes, as well as srebp1c, pparalpha, and ppargamma in adipose tissue. In WT mice, however, Acarbose treatment had little influence on weight gain and gene expression. Conclusions The results of this study suggest that long-term administration of Acarbose is effective for prevention of obesity and simple steatosis in SQSTM1-KO mice.

  • The α‐glucosidase inhibitor Acarbose prevents obesity and simple steatosis in sequestosome 1/A170/p62 deficient mice
    Hepatology Research, 2009
    Co-Authors: Kosuke Okada, Toru Yanagawa, Eiji Warabi, Keiko Yamastu, Junya Uwayama, Koichi Takeda, Hirotoshi Utsunomiya, Hiroshi Yoshida, Junichi Shoda, Tetsuro Ishii

    Abstract:

    AIM Sequestosome 1 (SQSTM1)/A170/p62 plays an important role in membrane-receptor mediated signal transduction and autophagic protein degradation. Although the mechanism involved is not clear, sqstm1 gene knockout (KO) mice develop mature-onset obesity and insulin resistance, leading to type II diabetes. KO mice show accumulation of fat in white adipose tissue and the liver when fed a standard diet. Acarbose is an alpha-glucosidase inhibitor that improves insulin sensitivity and decreases postprandial hyperglycemia, and it is used to treat type 2 diabetes. We examined whether or not dietary Acarbose prevented obesity and simple steatosis in KO mice. METHODS Wild-type (WT) and KO mice were fed a standard diet with or without Acarbose (0.8% w/w) from 15-25 weeks of age. The body weight and the fat content of adipose tissue and the liver were measured, and changes of lipid metabolism in these tissues were assessed from gene expression. RESULTS Acarbose treatment suppressed weight gain and the development of hepatic steatosis in KO mice. Acarbose treatment up-regulated hepatic expression of the pparalpha, ucp-2, and abca1 genes, as well as srebp1c, pparalpha, and ppargamma in adipose tissue. In WT mice, however, Acarbose treatment had little influence on weight gain and gene expression. CONCLUSIONS The results of this study suggest that long-term administration of Acarbose is effective for prevention of obesity and simple steatosis in SQSTM1-KO mice.

Kosuke Okada – One of the best experts on this subject based on the ideXlab platform.

  • the α glucosidase inhibitor Acarbose prevents obesity and simple steatosis in sequestosome 1 a170 p62 deficient mice
    Hepatology Research, 2009
    Co-Authors: Kosuke Okada, Toru Yanagawa, Eiji Warabi, Keiko Yamastu, Junya Uwayama, Koichi Takeda, Hirotoshi Utsunomiya, Hiroshi Yoshida, Junichi Shoda, Tetsuro Ishii

    Abstract:

    Aim Sequestosome 1 (SQSTM1)/A170/p62 plays an important role in membrane-receptor mediated signal transduction and autophagic protein degradation. Although the mechanism involved is not clear, sqstm1 gene knockout (KO) mice develop mature-onset obesity and insulin resistance, leading to type II diabetes. KO mice show accumulation of fat in white adipose tissue and the liver when fed a standard diet. Acarbose is an alpha-glucosidase inhibitor that improves insulin sensitivity and decreases postprandial hyperglycemia, and it is used to treat type 2 diabetes. We examined whether or not dietary Acarbose prevented obesity and simple steatosis in KO mice. Methods Wild-type (WT) and KO mice were fed a standard diet with or without Acarbose (0.8% w/w) from 15-25 weeks of age. The body weight and the fat content of adipose tissue and the liver were measured, and changes of lipid metabolism in these tissues were assessed from gene expression. Results Acarbose treatment suppressed weight gain and the development of hepatic steatosis in KO mice. Acarbose treatment up-regulated hepatic expression of the pparalpha, ucp-2, and abca1 genes, as well as srebp1c, pparalpha, and ppargamma in adipose tissue. In WT mice, however, Acarbose treatment had little influence on weight gain and gene expression. Conclusions The results of this study suggest that long-term administration of Acarbose is effective for prevention of obesity and simple steatosis in SQSTM1-KO mice.

  • The α‐glucosidase inhibitor Acarbose prevents obesity and simple steatosis in sequestosome 1/A170/p62 deficient mice
    Hepatology Research, 2009
    Co-Authors: Kosuke Okada, Toru Yanagawa, Eiji Warabi, Keiko Yamastu, Junya Uwayama, Koichi Takeda, Hirotoshi Utsunomiya, Hiroshi Yoshida, Junichi Shoda, Tetsuro Ishii

    Abstract:

    AIM Sequestosome 1 (SQSTM1)/A170/p62 plays an important role in membrane-receptor mediated signal transduction and autophagic protein degradation. Although the mechanism involved is not clear, sqstm1 gene knockout (KO) mice develop mature-onset obesity and insulin resistance, leading to type II diabetes. KO mice show accumulation of fat in white adipose tissue and the liver when fed a standard diet. Acarbose is an alpha-glucosidase inhibitor that improves insulin sensitivity and decreases postprandial hyperglycemia, and it is used to treat type 2 diabetes. We examined whether or not dietary Acarbose prevented obesity and simple steatosis in KO mice. METHODS Wild-type (WT) and KO mice were fed a standard diet with or without Acarbose (0.8% w/w) from 15-25 weeks of age. The body weight and the fat content of adipose tissue and the liver were measured, and changes of lipid metabolism in these tissues were assessed from gene expression. RESULTS Acarbose treatment suppressed weight gain and the development of hepatic steatosis in KO mice. Acarbose treatment up-regulated hepatic expression of the pparalpha, ucp-2, and abca1 genes, as well as srebp1c, pparalpha, and ppargamma in adipose tissue. In WT mice, however, Acarbose treatment had little influence on weight gain and gene expression. CONCLUSIONS The results of this study suggest that long-term administration of Acarbose is effective for prevention of obesity and simple steatosis in SQSTM1-KO mice.

Jean-louis Chiasson – One of the best experts on this subject based on the ideXlab platform.

  • Acarbose in the prevention of cardiovascular disease in subjects with impaired glucose tolerance and type 2 diabetes mellitus
    Current Opinion in Pharmacology, 2005
    Co-Authors: Sophie Delorme, Jean-louis Chiasson

    Abstract:

    The prevalence of glucose intolerance is increasing dramatically worldwide. Both impaired glucose tolerance (IGT) and type 2 diabetes are associated with excess mortality from cardiovascular disease. It is now generally accepted that these cardiovascular complications are related to prevailing hyperglycemia, particularly postprandial hyperglycemia. Acarbose specifically decreases the postprandial glycemic surge in IGT and diabetic subjects. The Study To Prevent Non-insulin-dependent Diabetes Mellitus (STOP-NIDDM) trial has shown that Acarbose treatment in IGT subjects decreased the risk of progression to diabetes by 36%. Furthermore, it was associated with a 49% risk reduction of cardiovascular events. In a subgroup of subjects, Acarbose treatment was accompanied by a 50% decrease in the progression of intima-media thickness of the carotids. Finally, a meta-analysis of seven major studies on the use of Acarbose in the treatment of diabetes indicated that Acarbose treatment was associated with a 35% risk reduction of cardiovascular disease. It is proposed that the mechanism by which Acarbose can lower the risk of cardiovascular events is through diminution of oxidative stress induced by postprandial glycemic excursion.

  • Acarbose in the treatment of elderly patients with type 2 diabetes.
    Diabetes research and clinical practice, 2003
    Co-Authors: Robert G. Josse, Jean-louis Chiasson, Edmond A. Ryan, David C.w. Lau, Stuart A. Ross, Jean-françois Yale, Lawrence A. Leiter, Pierre Maheux, Daniel Tessier, Thomas M. S. Wolever

    Abstract:

    Abstract Aims: To study the effect of Acarbose, an α-glucosidase inhibitor, on glycemic control in elderly patients with type 2 diabetes. Methods: Elderly patients with type 2 diabetes treated with diet alone were randomly treated in a double-blind fashion with placebo ( n =99) or Acarbose ( n =93) for 12 months. Results: After 12 months of therapy, there was a statistically significant difference in the change in glycated haemoglobin (HbA 1c ) (−0.6%) in the Acarbose group versus placebo, as well as in the incremental post-prandial glucose values (−2.1 mmol h/l) and mean fasting plasma glucose (−0.7 mmol/l). Although there was no effect of Acarbose on insulin release, there was a clear effect of Acarbose to decrease relative insulin resistance (−0.8) (HOMA method). In addition, Acarbose was generally well tolerated and safe in the elderly; most discontinuations were due to gastrointestinal side effects such as flatulence and diarrhea. There were no cases of hypoglycemia reported, and no clinically relevant changes in laboratory abnormalities or vital signs during the study. Conclusions: Acarbose improves the glycemic profile and insulin sensitivity in elderly patients with type 2 diabetes who are inadequately controlled on diet alone.

  • Acarbose for prevention of type 2 diabetes mellitus the stop niddm randomised trial
    The Lancet, 2002
    Co-Authors: Jean-louis Chiasson, M Hanefeld, Robert G. Josse, Ramon Gomis, Avraham Karasik, Markku Laakso

    Abstract:

    Summary Background The worldwide increase in type 2 diabetes mellitus is becoming a major health concern. We aimed to assess the effect of Acarbose in preventing or delaying conversion of impaired glucose tolerance to type 2 diabetes. Methods In a multicentre, placebo-controlled randomised trial, we randomly allocated patients with impaired glucose tolerance to 100 mg Acarbose or placebo three times daily. The primary endpoint was development of diabetes on the basis of a yearly oral glucose tolerance test (OGTT). Analyses were by intention to treat. Findings We randomly allocated 714 patients with impaired glucose tolerance to Acarbose and 715 to placebo. We excluded 61 (4%) patients because they did not have impaired glucose tolerance or had no postrandomisation data. 211 (31%) of 682 patients in the Acarbose group and 130 (19%) of 686 on placebo discontinued treatment early. 221 (32%) patients randomised to Acarbose and 285 (42%) randomised to placebo developed diabetes (relative hazard 0·75 [95% CI 0·63–0·90]; p=0·0015). Furthermore, Acarbose significantly increased reversion of impaired glucose tolerance to normal glucose tolerance (p Interpretation Acarbose could be used, either as an alternative or in addition to changes in lifestyle, to delay development of type 2 diabetes in patients with impaired glucose tolerance.