Diet-induced obesity in the rat: A model for gestational diabetes mellitus

Mar 26, 2004American journal of obstetrics and gynecology

Obesity caused by diet in rats as a model for pregnancy diabetes

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Abstract

Body weight in virgin rats on a cafeteria-style diet increased significantly after 4 weeks compared to control rats (P<.0001).

Increased body weight in cafeteria-style diet rats was due to a rise in fat mass as determined by body composition analysis.
Plasma leptin concentrations were elevated in both nonpregnant and pregnant cafeteria-style diet rats (P<.0001).
Nonpregnant cafeteria-style diet rats exhibited normal glucose levels but elevated insulin levels compared to control rats (P<.05 for insulin area under the curve).
Pregnant cafeteria-style diet rats demonstrated impaired glucose tolerance (P<.001) along with raised insulin levels (P<.05).
Fetal weight was similar between diet groups, but cafeteria-style diet rats had a higher litter weight due to increased litter size (P<.05).
Insulin resistance was observed in nonpregnant cafeteria-style diet rats and worsened during pregnancy, indicating a greater impact of obesity than pregnancy alone.

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OBJECTIVES: Obesity is one of the most important risk factors for the development of gestational diabetes mellitus (GDM). However, in obese women, it is difficult to disentangle the genetic and environmental contributions. The aim of this study was to investigate whether diet-induced obesity results in GDM in rats with the same genetic background.

STUDY DESIGN: Female Wistar rats were fed a cafeteria-style diet (CAF) or the standard control (C) diet from 70 days of age onward. After 4 weeks on the diets, subgroups of CAF and C rats were mated. In virgin and late-pregnant CAF and C rats, we determined body weight, body composition by dual-energy x-ray absorptiometry (DEXA), glucose tolerance by intravenous glucose tolerance test (IVGTT), and insulin sensitivity by hyperinsulinemic euglycemic clamp in nonanesthesized rats. Plasma leptin concentrations were also measured.

RESULTS: Body weight increased after 4 weeks in virgin CAF rats (P<.0001) and exceeded that of C rats throughout pregnancy. This resulted exclusively from increased fat mass, as determined by DEXA, and was associated with a rise in plasma leptin concentrations in nonpregnant and pregnant (both P<.0001) CAF rats. During the IVGTT, nonpregnant CAF rats showed normal glucose levels but increased insulin levels compared with C rats (P<.05 for the area under the curve for insulin: AUC(insulin)). In pregnant CAF animals, glucose tolerance was clearly impaired (AUC(glucose): P<.001) with insulin also raised (AUC(insulin): P<.05). On day 22, fetal weight was comparable between C and CAF rats, but litter weight was higher in CAF rats (P<.05) owing to an increase in litter size. Hyperinsulinemic clamp studies revealed unequivocal insulin resistance in nonpregnant CAF rats, which was aggravated by pregnancy, the proportional effect of obesity being higher than that of pregnancy.

CONCLUSION: Diet-induced obesity in rats is associated with glucose intolerance during pregnancy but not in the nonpregnant state. This is likely to result from the additive effects of obesity and pregnancy on insulin sensitivity. This obese rat model is an attractive model to study further the physiologic and molecular abnormalities in GDM.

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Diet-induced obesity in the rat: A model for gestational diabetes mellitus

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