Metabolism
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* Dữ liệu chỉ mang tính chất tham khảo
Sắp xếp:
Regulation of the glutamate dehydrogenase activity in rat islets of Langerhans and its consequence on insulin release
Metabolism - Tập 43 - Trang 1187-1195 - 1994
Lower androgenicity is associated with higher plasma levels of prothrombotic factors irrespective of age, obesity, body fat distribution, and related metabolic parameters in men
Metabolism - Tập 46 - Trang 1287-1293 - 1997
Effect of angiotensin-converting enzyme inhibition with perindopril and β-blockade with atenolol on retinal blood flow in hypertensive diabetic subjects
Metabolism - Tập 47 - Trang 28-33 - 1998
Basal peroxisome proliferator activated receptor gamma coactivator 1α expression is independent of calcineurin in skeletal muscle
Metabolism - Tập 61 - Trang 389-394 - 2012
Diisopropylammonium dichloroacetate: Regulation of metabolic intermediates in muscle of alloxan diabetic rats
Metabolism - Tập 20 - Trang 830-834 - 1971
Riboflavin nutritional status and flavoprotein enzymes in normal and genetically diabetic KK mice
Metabolism - Tập 27 - Trang 531-537 - 1978
Hexokinase isozymes of normal human subcutaneous adipose tissue
Metabolism - Tập 27 - Trang 1101-1108 - 1978
β-cell function during insulin-modified intravenous glucose tolerance test successfully assessed by the C-peptide minimal model
Metabolism - Tập 48 - Trang 1162-1166 - 1999
Non-insulin-dependent diabetes mellitus, abnormal lipoprotein metabolism, and atherosclerosis
Metabolism - Tập 36 Số 2 - Trang 1-8 - 1987
Increased insulin sensitivity and decreased insulin secretion in offspring of insulin-sensitive type 2 diabetic patients
Metabolism - Tập 49 - Trang 1219 - 2000
To investigate the early defects of glucose metabolism in insulin-sensitive type 2 diabetes, we performed oral and frequently sampled intravenous glucose tolerance tests (OGTT and FSIGT) with minimal model analysis in 15 offspring of Japanese type 2 diabetics with normal insulin sensitivity (insulin resistance index of homeostasis model assessment [HOMA-R] < 2.0) and in 20 healthy control subjects without a family history of type 2 diabetes. The frequency of impaired glucose tolerance (IGT) was 40% (6 of 15) in the offspring and 0% (0 of 20) in the controls. Fasting plasma glucose (4.8 ± 0.1 v 4.6 ± 0.1 mmol/L, P = .18) and immunoreactive insulin ([IRI] 29.9 ± 2.5 v 28.3 ± 2.5 pmol/L, P ± = .64) were comparable between the offspring and the controls. The rate of glucose disappearance (KG) was significantly lower in the offspring versus the control group (2.00 ± 0.22 v 2.60 ± 0.17 min−1, P = .03). The insulin sensitivity index (Si) was significantly greater in the offspring versus the controls (2.68 ± 0.41 v 1.71 ± 0.17 × 10−4 · min−1 · pmol/L, P = .02). First-phase insulin secretion (FPI) to intravenous glucose was significantly lower in the offspring versus the control group (886 ± 110 v 2,296 ± 267 min · pmol/L, P < .01). Glucose effectiveness (SG) was comparable between the offspring and control groups. The disposition index (Si × FPI) was significantly lower in the offspring versus the controls (2,106 ± 256 v 3,652 ± 490 × 10−4, P = .02). When the offspring were subdivided into 2 groups by glucose tolerance status, both normal glucose tolerance (NGT) offspring and IGT offspring showed a significant decrease in FPI and increase in Si. Thus, although the offspring of insulin-sensitive type 2 diabetics had increased insulin sensitivity, the impairment in insulin secretion was more dominant. Our results suggest that the early metabolic abnormality in insulin-sensitive type 2 diabetes is an insulin secretory dysfunction despite increased insulin sensitivity.
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