Characterization of plasma lipids in genetically obese mice: the mutants obese, diabetes, fat, tubby, and lethal yellow

PM Nishina, S Lowe, J Wang, B Paigen - Metabolism, 1994 - Elsevier
PM Nishina, S Lowe, J Wang, B Paigen
Metabolism, 1994Elsevier
Plasma lipid levels were measured in control strains C57BL 6J (B6) and C57BL KsJ (BKs)
and in the mutants obese (ob), diabetes (db), fat (fat), tubby (tub), and lethal yellow (A y),
which are considered models of non-insulin-dependent diabetes mellitus (NIDDM), to
determine if perturbations in plasma lipids were similar to those observed in the obese or
diabetic human population. Compared with control mice, obese, diabetes, tubby, and lethal
yellow mice had triglyceride levels that were elevated 1.5-fold to twofold, but fat mice had …
Plasma lipid levels were measured in control strains C57BL 6J (B6) and C57BL KsJ (BKs) and in the mutants obese (ob), diabetes (db), fat (fat), tubby (tub), and lethal yellow (A y), which are considered models of non-insulin-dependent diabetes mellitus (NIDDM), to determine if perturbations in plasma lipids were similar to those observed in the obese or diabetic human population. Compared with control mice, obese, diabetes, tubby, and lethal yellow mice had triglyceride levels that were elevated 1.5-fold to twofold, but fat mice had triglyceride levels similar to those of controls. Elevated plasma cholesterol levels, which were also observed in most mutant mice, were mainly due to an increase in high-density lipoprotein cholesterol (HDL-C). The degree of hypercholesterolemia appeared to be related to the age of onset and severity of the obesity and diabetes phenotype, with the greatest elevations occurring in obese and diabetes, milder elevations in fat mice of both sexes, male tubby, and male yellow mice, and no apparent changes in female tubby or lethal yellow mice. Plasma HDL-C and glucose levels and body weight in B 6-db db mice and their normal littermates were measured at intervals between 2 and 12 weeks of age to determine when the changes in cholesterol occurred in relationship to hyperglycemia and obesity. An elevation in HDL-C in B6-db db mice was apparent by 3 weeks of age, a time concurrent with the elevation in blood glucose but before any weight differences. We conclude that mice carrying mutations that confer a phenotype similar to human NIDDM show an elevation in plasma triglycerides and cholesterol comparable to that observed in humans. However, in mice the increase in total cholesterol is due to HDL-C, the primary cholesterol carrier in mice fed a commercially prepared stock diet containing 4% fat.
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