期刊
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
卷 293, 期 6, 页码 E1730-E1735出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00572.2007
关键词
etiology; insulin secretory defects; insulin resistance; mathematical modeling
Both male Zucker Fatty (mZF) and lower-fat-fed female Zucker diabetic fatty (LF-fZDF) rats are obese but remain normoglycemic. Male ZDF (mZDF) and highfatfed female ZDF rats (HF-fZDF) are also obese but develop diabetes between 7 and 10 wk of age. Although these models have been well studied, the mechanisms governing the adaptations to obesity in the normoglycemic animals, and the failure of adaptation in the animals that develop diabetes, remain unclear. Here we use quantitative morphometry and our recently developed coupled beta-cell mass (beta(m)), insulin, and glucose model to elucidate the dynamics of insulin sensitivity (S-I), beta-cell secretory capacity (beta(sc)), and beta(m) in these four animal models. Both groups that remained normoglycemic with increasing obesity (mZF, LF-fZDF) exhibited increased beta(m) and constant beta(sc) in response to a falling S-I. In rats that developed hyperglycemia (mZDF, HF-fZDF), there was a greater reduction in S-I and slower expansion of beta(m), with constant beta(sc). beta(sc) decreased after glucose levels rose above 20 mM. Taken together, these data suggest that excessive insulin resistance and insufficient beta(m) adaptation play a primary role in the pathogenesis of diabetes.
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