Family history of diabetes mellitus determines insulin sensitivity and beta cell function in polycystic ovary syndrome
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
17705674
DOI
10.33549/physiolres.931275
PII: 1275
Knihovny.cz E-zdroje
- MeSH
- antropometrie MeSH
- arginin metabolismus MeSH
- beta-buňky fyziologie MeSH
- buňky vylučující glukagon fyziologie MeSH
- diabetes mellitus 2. typu genetika MeSH
- diabetes mellitus genetika patofyziologie MeSH
- dospělí MeSH
- glykemický clamp MeSH
- homeostáza MeSH
- hormony krev MeSH
- index tělesné hmotnosti MeSH
- inzulinová rezistence genetika MeSH
- krevní glukóza metabolismus MeSH
- krevní tlak fyziologie MeSH
- lidé MeSH
- syndrom polycystických ovarií genetika patofyziologie MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- arginin MeSH
- hormony MeSH
- krevní glukóza MeSH
To examine the impact of family history of diabetes mellitus 2 (DM 2) on insulin sensitivity and secretion in lean women with polycystic ovary syndrome (PCOS). Thirteen healthy women (C), 14 PCOS without family history of DM 2 (FH-) and 8 PCOS with family history of DM 2 (FH+) were examined using euglycemic hyperinsulinemic clamp and an arginine secretion test (insulin and glucagon at fasting glycemia (AIR(FG) and AGR(FG)) and at hyperglycemia (AIR(14) and AGR(14)). FH+ women were more insulin resistant than FH- with lower insulin sensitivity index corrected per lean body mass (p 0.05). They had significantly higher triglycerides (p 0.05) and lower HDL-cholesterol (p 0.05) than C or FH- women. Concerning insulin secretion, AIR(FG) was increased in FH+ women comparing FH- women (p 0.05). Disposition indices derived from AIR(FG) or AIR(14) and insulin sensitivity index did not differ between FH+ or FH-. Thus, women with PCOS with the concomitant family history of DM 2 have lower insulin sensitivity than healthy control women. Insulin resistance observed in these women with PCOS is compensated by increased insulin secretion.
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