[Glucose tolerance, function of pancreatic B-cells and blood lipids in "healthy" offspring of parents with conjugal type 2 diabetes].
In 56 adult normoglycemic nondiabetic (WHO criteria) subjects, whose both parents had type 2 diabetes, and in 68 control probants, matched for age, sex and body mass without family history of diabetes, the OGTT (75 g) was carried out, including measurement of serum insulin (IRI) and C-peptide (CP). In fasting state also the blood lipid profile was determined: serum triglycerides, total cholesterol, LDL-cholesterol, HDL-cholesterol, apolipoprotein AI (apoAI) and apolipoprotein B (apoB). In comparison with the control group, the offspring had significantly lower mean glycaemia on fasting, and non significantly elevated from the 60 min of the test, the significantly higher values of serum IRI and CP in fasting state and at the end of the test (120-180 min), and significantly lower serum CP:IRI molar ratio, expressing the reduced hepatic clearance of insulin. The offspring had significantly higher mean values of serum LDL-cholesterol, and significantly lower of serum HDL-cholesterol and apoAI, not disclosing significant differences in the serum levels of triglycerides, total cholesterol and apoB with the control group. Only serum HDL-cholesterol was significantly (negatively) correlated wit serum IRI and CP-values. The covariance analysis, eliminating the influence of age, body mass and the secretory activity of pancreatic B-cells, revealed the significant correlation of the presence of parental diabetes with serum levels of LDL-cholesterol (increase), and HDL-cholesterol and apoAI (decrease) in the offspring. These results prove indirectly, that in subjects genetically predisposed to type 2 diabetes, before the manifestation of glucose intolerance are present other effects of insulin resistance, expressed in increased activity of pancreatic B-cells, increased transfer of insulin to extrahepatic tissues, and in changes of concentration/composition of some lipoproteins dues to reduced influence of insulin on the enzymes which control their metabolism.
Jaskólska-Ładosz
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III Oddział Chorób Wewnetrznych i Diabetologii Centralnego Szpitala Klinicznego MSWiA w Warszawie.
Kasperska-Czyzykowa
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Stepień
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Nowaczyk
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D000328:Adult; D016632:Apolipoprotein A-I / Q000097:blood; D001055:Apolipoproteins B / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism*; D002096:C-Peptide / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics* / Q000378:metabolism; D005260:Female; D020022:Genetic Predisposition to Disease; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000097:blood; D007515:Islets of Langerhans / Q000378:metabolism*; D008055:Lipids / Q000097:blood*; D008297:Male; D014280:Triglycerides / Q000097:blood
D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D001786:Blood Glucose; D002096:C-Peptide; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D007328:Insulin; D008055:Lipids; D014280:Triglycerides