Differences in Insulin Action and Secretion, Plasma Lipids and Blood Pressure Levels between Impaired Fasting Glucose and Impaired Glucose Tolerance in Japanese Subjects

Miyazaki, Yoshinori; Akasaka, Hiroshi; Ohnishi, Hirofumi; Saitoh, Shigeyuki; DeFronzo, Ralph A.; Shimamoto, Kazuaki

doi:10.1291/hypres.31.1357

Cited by 18 publications

(8 citation statements)

References 36 publications

(15 reference statements)

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“…Therefore, besides alleviation of glucose and / or lipotoxicity toxicity, VG could directly improve hepatic insulin resistance and augment the benefi cial eff ects of NAT on postprandial dysmetabolism in our insulin-resistant animal models. Consistent with the fi ndings that hepatic insulin resistance is the major determining factor on fasting plasma glucose levels [22] , fasting plasma glucose in the combination group is lower compared to the monotherapies, but there is no significant diff erence between them. High data variability of fasting plasma glucose levels may aff ect the statistical signifi cance.…”

supporting

confidence: 85%

Combination Therapy with Nateglinide and Vildagliptin Improves Postprandial Metabolic Derangements in Zucker Fatty Rats

Miura

Kitahara²,

Yamagishi³

2010

Horm Metab Res

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Postprandial metabolic derangements are one of the risk factors of cardiovascular disease in humans. Insulin resistance and/or impaired early-phase insulin secretion are major determinants of postprandial metabolic derangements. In this study, we investigated the potential utility of combination therapy with vildagliptin, a dipeptidyl peptidase IV (DPP-IV) inhibitor and nateglinide, a rapid-onset/short-duration insulinotropic agent, for the treatment of postprandial metabolic derangements in Zucker Fatty (ZF) rats, an animal model of obesity with insulin resistance. ZF rats fed twice daily with or without high fat diet (HFD) were given vehicle, 50 mg/kg of nateglinide, 10 mg/kg of vildagliptin, or both for 6 weeks. Combination therapy with nateglinide and vildagliptin for 2 weeks ameliorated postprandial hyperglycemia, hypertriglyceridemia, and elevation of free fatty acid in ZF rats fed with HFD. 6-week treatment with nateglinide and vildagliptin not only increased hepatic levels of phosphorylated forkhead box protein 1A (FOXO1A), but also reduced triglyceride contents in the liver. Combination therapy also prevented the loss of pancreatic islet mass in ZF rats fed with HFD. These observations demonstrate that combination therapy with nateglinide and vildagliptin may improve postprandial metabolic derangements probably by ameliorating early phase of insulin secretion and hepatic insulin resistance, respectively, in ZF rats fed with HFD. Since combination therapy with nateglinide and vildagliptin restored the decrease in pancreatic beta cell mass, our present findings suggest that combination therapy could be a promising therapeutic strategy for postprandial dysmetabolism associated with obese and insulin resistance.

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supporting

confidence: 85%

Combination Therapy with Nateglinide and Vildagliptin Improves Postprandial Metabolic Derangements in Zucker Fatty Rats

Miura

Kitahara²,

Yamagishi³

2010

Horm Metab Res

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“…Another study reported that isolated IGT was characterized by both impaired insulin secretion and insulin resistance, but there are no significant differences in insulin sensitivity between isolated IFG and isolated IGT ( n = 128, n = 55, resp.) subjects [ 24 ]. In the present study, we have elucidated the significant difference between isolated IGT and isolated IFG with large number of subjects.…”

Section: Discussionmentioning

confidence: 99%

Insulin Secretory Defect and Insulin Resistance in Isolated Impaired Fasting Glucose and Isolated Impaired Glucose Tolerance

Aoyama-Sasabe

Fukushima

Xin

et al. 2016

Journal of Diabetes Research

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Objective. To investigate the characteristics of isolated impaired glucose tolerance (IGT) and isolated impaired fasting glucose (IFG), we analyzed the factors responsible for elevation of 2-hour postchallenge plasma glucose (2 h PG) and fasting plasma glucose (FPG) levels. Methods. We investigated the relationship between 2 h PG and FPG levels who underwent 75 g OGTT in 5620 Japanese subjects at initial examination for medical check-up. We compared clinical characteristics between isolated IGT and isolated IFG and analyzed the relationships of 2 h PG and FPG with clinical characteristics, the indices of insulin secretory capacity, and insulin sensitivity. Results. In a comparison between isolated IGT and isolated IFG, insulinogenic index was lower in isolated IGT than that of isolated IFG (0.43 ± 0.34 versus 0.50 ± 0.47, resp.; p < 0.01). ISI composite was lower in isolated IFG than that of isolated IGT (6.87 ± 3.38 versus 7.98 ± 4.03, resp.; p < 0.0001). In isolated IGT group, insulinogenic index showed a significant correlation with 2 h PG (r = −0.245, p < 0.0001) and had the strongest correlation with 2 h PG (β = −0.290). In isolated IFG group, ISI composite showed a significant correlation with FPG (r = −0.162, p < 0.0001) and had the strongest correlation with FPG (β = −0.214). Conclusions. We have elucidated that decreased early-phase insulin secretion is the most important factor responsible for elevation of 2 h PG levels in isolated IGT subjects, and decreased insulin sensitivity is the most important factor responsible for elevation of FPG levels in isolated IFG subjects.

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“…This measure of the disposition index was reduced in iIFG (mean ± SEM, 7.1 ± 0.5; P < 0.05; with iIFG defined as fasting plasma glucose 6.1–7.0 mmol/L) compared with the NGT group (9.7 ± 0.2). A more extreme and statistically significant difference was detected in the iIGT (mean ± SEM, 2.7 ± 0.2) and the combined IFG plus IGT (2.1 ± 0.2) groups compared with both the NGT and iIFG groups ( P < 0.05) (33). In another study of 1,272 Chinese adults, a decline in early phase DI o (ΔAUC PI /ΔAUC PG at 30 min, adjusted with the Matsuda Index) was found in both iIFG (fasting glucose 5.6–7.0 mmol/L) and iIGT—both significantly lower than NGT—but DI o in iIGT also was significantly lower than DI o in IFG (both P < 0.05) (34).…”

Section: Discussionmentioning

confidence: 99%

Evidence of Reduced β-Cell Function in Asian Indians With Mild Dysglycemia

et al. 2013

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OBJECTIVETo examine β-cell function across a spectrum of glycemia among Asian Indians, a population experiencing type 2 diabetes development at young ages despite low BMI.RESEARCH DESIGN AND METHODSOne-thousand two-hundred sixty-four individuals without known diabetes in the Diabetes Community Lifestyle Improvement Program in Chennai, India, had a 75-g oral glucose tolerance test, with glucose and insulin measured at 0, 30, and 120 min. Type 2 diabetes, isolated impaired fasting glucose (iIFG), isolated impaired glucose tolerance (iIGT), combined impaired fasting glucose and impaired glucose tolerance, and normal glucose tolerance (NGT) were defined by American Diabetes Association guidelines. Measures included insulin resistance and sensitivity (homeostasis model assessment of insulin resistance [HOMA-IR], modified Matsuda Index, 1/fasting insulin) and β-cell function (oral disposition index = [Δinsulin0–30/Δglucose0–30] × [1/fasting insulin]).RESULTSMean age was 44.2 years (SD, 9.3) and BMI 27.4 kg/m2 (SD, 3.8); 341 individuals had NGT, 672 had iIFG, IGT, or IFG plus IGT, and 251 had diabetes. Patterns of insulin resistance or sensitivity were similar across glycemic categories. With mild dysglycemia, the absolute differences in age- and sex-adjusted oral disposition index (NGT vs. iIFG, 38%; NGT vs. iIGT, 32%) were greater than the differences in HOMA-IR (NGT vs. iIFG, 25%; NGT vs. iIGT, 23%; each P < 0.0001). Compared with NGT and adjusted for age, sex, BMI, waist circumference, and family history, the odds of mild dysglycemia were more significant per SD of oral disposition index (iIFG: odds ratio [OR], 0.36; 95% CI, 0.23–0.55; iIGT: OR, 0.37; 95% CI, 0.24–0.56) than per SD of HOMA-IR (iIFG: OR, 1.69; 95% CI, 1.23–2.33; iIGT: OR, 1.53; 95% CI, 1.11–2.11).CONCLUSIONSAsian Indians with mild dysglycemia have reduced β-cell function, regardless of age, adiposity, insulin sensitivity, or family history. Strategies in diabetes prevention should minimize loss of β-cell function.

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Differences in Insulin Action and Secretion, Plasma Lipids and Blood Pressure Levels between Impaired Fasting Glucose and Impaired Glucose Tolerance in Japanese Subjects

Cited by 18 publications

References 36 publications

Combination Therapy with Nateglinide and Vildagliptin Improves Postprandial Metabolic Derangements in Zucker Fatty Rats

Combination Therapy with Nateglinide and Vildagliptin Improves Postprandial Metabolic Derangements in Zucker Fatty Rats

Insulin Secretory Defect and Insulin Resistance in Isolated Impaired Fasting Glucose and Isolated Impaired Glucose Tolerance

Evidence of Reduced β-Cell Function in Asian Indians With Mild Dysglycemia

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