Glucose turnover and adipose tissue lipolysis are insulin-resistant in healthy relatives of type 2 diabetes patients: is cellular insulin resistance a secondary phenomenon?

التفاصيل البيبلوغرافية
العنوان: Glucose turnover and adipose tissue lipolysis are insulin-resistant in healthy relatives of type 2 diabetes patients: is cellular insulin resistance a secondary phenomenon?
المؤلفون: Marian Wysocki, Per-Anders Jansson, Jan W. Eriksson, Finn Waagstein, Ulf Smith
المصدر: Diabetes. 48:1572-1578
بيانات النشر: American Diabetes Association, 1999.
سنة النشر: 1999
مصطلحات موضوعية: Adult, Male, medicine.medical_specialty, Lipolysis, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Glucose uptake, Adipose tissue, Cell Separation, Type 2 diabetes, Biology, Insulin resistance, Reference Values, Internal medicine, Adipocytes, Internal Medicine, medicine, Humans, Insulin, Glucose tolerance test, medicine.diagnostic_test, Glucose Tolerance Test, Glucose clamp technique, medicine.disease, Blood, Glucose, Endocrinology, Adipose Tissue, Diabetes Mellitus, Type 2, Exercise Test, Glucose Clamp Technique, Female, Insulin Resistance
الوصف: To elucidate potential mechanisms for insulin resistance occurring early in the development of type 2 diabetes, we studied 10 young healthy individuals, each with two first-degree relatives with type 2 diabetes, and 10 control subjects without known type 2 diabetic relatives. They were pairwise matched for age (35 +/- 1 vs. 35 +/- 1 years), BMI (23.6 +/- 0.6 vs. 23.1 +/- 0.4 kg/m2), and sex (four men, six women). Glucose turnover was assessed during a euglycemic clamp at two insulin levels (low approximately 20 mU/l; high approximately 90 mU/l), and abdominal subcutaneous adipose tissue (SAT) lipolysis and blood flow were concomitantly studied with microdialysis and 133Xe clearance. HbA1c was higher in patients with type 2 diabetic relatives than in control subjects (4.8 +/- 0.1 vs. 4.5 +/- 0.1%, P < 0.02), but fasting glucose, insulin, and C-peptide levels were similar. During the clamp, the insulin sensitivity index for glucose disposal was lower (P < 0.03) in relatives than in control subjects (low 12.0 +/- 1.6 vs. 18.1 +/- 1.4; high 9.4 +/- 0.8 vs. 12.9 +/- 0.6 [100 x mg x l x kg(-1) x mU(-1) x min(-1)]). This difference was partially attributed to slightly higher clamp insulin levels in the relatives (P < 0.03), suggesting an impaired rate for insulin clearance. SAT lipolysis measured as in situ glycerol release did not differ under basal conditions (2.0 +/- 0.2 vs. 2.1 +/- 0.2 micromol x kg(-1) x min(-1)), but the suppression during the insulin infusion was less marked in relatives than in control subjects (glycerol release: low 0.92 +/- 0.09 vs. 0.68 +/- 0.16; high 0.71 +/- 0.10 vs. 0.34 +/- 0.10 micromol x kg(-1) x min(-1); P < 0.03). Plasma nonesterified fatty acids also tended to be higher in relatives than in control subjects during the insulin infusion (NS). In contrast, in vitro experiments with isolated subcutaneous adipocytes displayed similar effects of insulin in relatives and control subjects with respect to both glucose uptake and antilipolysis. In conclusion, insulin action in vivo on both lipolysis and glucose uptake is impaired early in the development of type 2 diabetes. Since this impairment was not found in isolated adipocytes, it may be suggested that neural or hormonal perturbations precede cellular insulin resistance in type 2 diabetes.
تدمد: 1939-327X
0012-1797
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::487431a9761b80cac3f7bec314e991f8Test
https://doi.org/10.2337/diabetes.48.8.1572Test
رقم الانضمام: edsair.doi.dedup.....487431a9761b80cac3f7bec314e991f8
قاعدة البيانات: OpenAIRE