The importance of diabetes heredity in lean subjects on insulin secretion, blood lipids and oxygen uptake in the pathogenesis of glucose intolerance - PubMed (original) (raw)

PMID: 3527520

Comparative Study

The importance of diabetes heredity in lean subjects on insulin secretion, blood lipids and oxygen uptake in the pathogenesis of glucose intolerance

K Berntorp et al. Diabetes Res. 1986 Jun.

Abstract

Insulin secretion, work capacity and plasma lipids were evaluated in 52 middle-aged men with impaired glucose tolerance (IGT), and the values were compared with those of 23 normoglycemic subjects with family histories of Type 2 diabetes and of 22 non-hereditary normoglycemic controls. All subjects were non-obese males of comparable age. Estimated maximal oxygen uptake was significantly lower (p less than 0.01) and triglyceride concentrations significantly higher (p less than 0.01) in IGT individuals than in subjects of the non-hereditary normoglycemic group, while no significant differences were noted in comparison with the hereditary group. IGT individuals showed an impaired insulin response to glucose with significantly lower absolute values of insulin and C-peptide during the early phase of the oral glucose tolerance test (OGTT) than in non-hereditary normoglycemic subjects, but not significantly lower than in the hereditary group. Similarly, at most time points of the OGTT the ratios of insulin and C-peptide to glucose were significantly lower in the IGT group than in the non-hereditary group, while these differences were less pronounced in comparison with the hereditary group. These findings suggest some similarities of metabolic disturbances in lean normoglycemics with positive family histories of Type 2 diabetes and in lean IGT individuals. Family history of diabetes (both first degree and second degree only) was significantly more prevalent among IGT individuals than among normals.

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The importance of diabetes heredity in lean subjects on insulin secretion, blood lipids and oxygen uptake in the pathogenesis of glucose intolerance - PubMed (original) (raw)