Pathogenesis of type 2 diabetes mellitus

Dostou, Jean M.; Gerich, John E.

doi:10.1055/s-2001-18577

Cited by 16 publications

(17 citation statements)

References 41 publications

(60 reference statements)

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“…However, they disagree with the decreased capacity of insulin secretion to a glucose challenge in the offspring born to WNIN rat dams on magnesium and zinc deficiencies (Venu et al 2005, 2008, Padmavathi et al 2009. Considering that IR and/or altered insulin secretion exist before the onset of fasting and postprandial hyperglycemia which lead to type 2 diabetes (Weyer et al 1999, Dostou & Gerich 2001, our findings suggest the predisposal of the CrR offspring to type 2 diabetes. The finding that the changes observed at 9 months of age were not seen later in male offspring is in agreement with our similar findings in Mg restricted rat offspring (Venu et al 2008).…”

Section: Discussionmentioning

confidence: 56%

Impact of maternal chromium restriction on glucose tolerance, plasma insulin and oxidative stress in WNIN rat offspring

Padmavathi¹,

Rao²,

Raghunath³

2011

Journal of Molecular Endocrinology

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Robust evidence suggests that nutritional insult during fetal development could program the offspring to glucose intolerance, impaired insulin response and insulin resistance (IR). Considering the importance of chromium (Cr) in maintaining carbohydrate metabolism, this study determined the effect of maternal Cr restriction (CrR) on glucose metabolism and plasma insulin in Wistar/NIN (WNIN) rat offspring and the associated biochemical and/or molecular mechanisms. Female, weanling WNIN rats received ad libitum for 12 weeks, a control diet or the same with 65% restriction of Cr and mated with control males. Some of the Cr-restricted dams were rehabilitated from conception or parturition and their pups weaned on to control diet. At the time of weaning, half of the Cr restricted offspring were rehabilitated to control diet while others continued on Cr-restricted diet. Maternal CrR increased fasting plasma glucose, fasting insulin, homeostasis model assessment of IR, and area under the curve of glucose and insulin during oral glucose tolerance test in the offspring. Expression and activity of rate-limiting enzymes of glucose metabolism were comparable among different groups and expression of genes involved in insulin secretion was increased albeit in male offspring whereas antioxidant enzyme activities were decreased in offspring of both genders. Rehabilitation, in general, corrected the changes albeit partially. Maternal dietary CrR induced IR, impaired glucose tolerance in WNIN rat offspring and was associated with increased oxidative stress, which may predispose them to type 2 diabetes in their later life.

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Section: Discussionmentioning

confidence: 56%

Impact of maternal chromium restriction on glucose tolerance, plasma insulin and oxidative stress in WNIN rat offspring

Padmavathi¹,

Rao²,

Raghunath³

2011

Journal of Molecular Endocrinology

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“…Type 2 diabetes is a chronic metabolic disorder, currently affecting 140-150 million people worldwide, which often leads to long-term microvascular and macrovascular complications that substantially increase morbidity and mortality [1].…”

Section: Introductionmentioning

confidence: 99%

Lower within‐subject variability of fasting blood glucose and reduced weight gain with insulin detemir compared to NPH insulin in patients with type 2 diabetes

Haak

Tiengo

Draeger

et al. 2004

Diabetes Obesity Metabolism

245

165

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“…Although most attention has focused on the increase in type 2 diabetes, there has been a parallel increase in type 1 diabetes, which requires explanation (1). Type 2 diabetes is believed to result from the loss of ␤-cell function in association with insulin resistance (2). The Accelerator Hypothesis regards type 1 diabetes in the same way (3).…”

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confidence: 99%

Testing the Accelerator Hypothesis

et al. 2003

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OBJECTIVE -Previous reports have predicted greater risk of type 1 diabetes among people who were heavier as young children. The Accelerator Hypothesis predicts earlier onset in heavier people, without necessarily a change in risk, and views type 1 and type 2 diabetes as the same disorder of insulin resistance, set against different genetic backgrounds. Insulin resistance is a function of fat mass, and increasing body weight in the industrialized world has been accompanied by earlier presentation (i.e., acceleration) of type 2 diabetes. We wanted to establish whether increasing body weight was also asociated with the earlier presentation of type 1 diabetes, as the Accelerator Hypothesis would predict.RESEARCH DESIGN AND METHODS -The relationships between fatness and age at diagnosis were examined in context of birth weight, weight change since birth, weight at diagnosis, BMI at diagnosis, and BMI 12 months later in 94 children aged 1-16 years (49 boys and 45 girls) presenting for management of acute-onset type 1 diabetes.RESULTS -BMI standard deviation score (SDS) at diagnosis, weight SDS change since birth, and BMI SDS 12 months later were all inversely related to age at presentation (r ϭ Ϫ0.39 to Ϫ0.40, P Ͻ 0.001). The boys were significantly fatter than the girls (BMI SDS 0.56 vs. Ϫ0.08, respectively; P ϭ 0.006) and presented with diabetes at a significantly younger age (6.74 vs. 8.32 years, respectively; P Ͻ 0.05). The sex difference in age at diagnosis, however, disappeared when corrected for BMI (P ϭ 0.31), suggesting that fatness or something related to it was the responsible factor.CONCLUSIONS -The data are consistent with the hypothesis that the age at presentation of type 1 diabetes is associated with fatness. The implications for prevention of type 1 diabetes may be important. Diabetes Care 26:2865-2870, 2003T he prevalence of diabetes is increasing rapidly in industrialized countries. Although most attention has focused on the increase in type 2 diabetes, there has been a parallel increase in type 1 diabetes, which requires explanation (1). Type 2 diabetes is believed to result from the loss of ␤-cell function in association with insulin resistance (2). The Accelerator Hypothesis regards type 1 diabetes in the same way (3).Awareness of overlap between type 1 and type 2 diabetes is not new. There has long been interest in insulin resistance in type 1 diabetes, although related more to its implications for management and outcome than to its pathogenesis (4 -8). The term "type one-and-a-half" diabetes, referring to the progression in some from type 2 to type 1 diabetes, was coined years ago and remains an area of lively debate (9). In a modern context, the increasing difficulty in distinguishing type 1 from type 2 diabetes in obese young people has given rise to the designation "double diabetes," in which recognition is given to the coexistence of autoimmunity and insulin resistance (10).The insulin resistance that underlies type 2 diabetes seems to result mainly from lifestyle factors: weight increase a...

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Pathogenesis of type 2 diabetes mellitus

Cited by 16 publications

References 41 publications

Impact of maternal chromium restriction on glucose tolerance, plasma insulin and oxidative stress in WNIN rat offspring

Impact of maternal chromium restriction on glucose tolerance, plasma insulin and oxidative stress in WNIN rat offspring

Lower within‐subject variability of fasting blood glucose and reduced weight gain with insulin detemir compared to NPH insulin in patients with type 2 diabetes

Testing the Accelerator Hypothesis

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