Effects of dietary carbohydrates on glucose and lipid metabolism in golden Syrian hamsters

Siddika E Karakas, Heidi Vriend, Rogelio Almario, Lap Chi Chow, Michael N. Goodman

Research output: Contribution to journalArticle

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Abstract

Frequent coexistence of insulin resistance, central obesity, and hypertriglyceridemia in the same individual suggests an underlying common pathogenesis. Insulin resistance and hypertriglyceridemia can be induced by carbohydrate feeding in rats. Golden Syrian hamsters are believed to be resistant to the metabolic effects of dietary carbohydrates. We investigated the effects of diets containing 60% fructose or sucrose on glucose and lipid metabolism in hamsters, both in the fasting state and during an intravenous glucose tolerance test. Fructose caused obesity (weight after treatment: 131 ± 7 gm in the control group, 155 ± 5 gm in the fructose group, 136 ± 7 gm in sucrose group, p < 0.04). Fructose also reduced glucose disappearance rate (K(G): 2.69% ± 0.39% in the control group, 1.45% ± 0.18% in the fructose group, p < 0.02). Sucrose caused a marginal decrease in glucose disappearance (K(G): 1.93% ± 0.21%, p = 0.08 vs the control group). Only fructose feeding increased fasting plasma nonesterified fatty acids (0.645 ± 0.087 mEq/L in the control group, 1.035 ± 0.083 mEq/L in the fructose group, 0.606 ± 0.061 mEq/L in the sucrose group, p < 0.002), plasma triglycerides (84 ± 6 mg/dl in the control group, 270 ± 65 mg/dl in the fructose group, 94 ± 16 mg/dl in the sucrose group, p < 0.0002), and liver triglycerides (1.88 ± 0.38 mg/gm liver weight in the control group, 2.35 ± 0.24 mg/gm in the fructose group, 1.41 ± 0.13 mg/gm in the sucrose group, p < 0.04). Previous studies in the rat have suggested that dietary carbohydrates induce insulin resistance by increasing plasma nonesterified fatty acids and triglycerides, which are preferentially used by the muscles. The present report shows that sucrose also can cause some decrease in glucose disappearance in the hamster without causing hypertriglyceridemia or increasing plasma nonesterified fatty acids. Thus other mechanisms may also contribute to the insulin resistance in the hamster. These findings suggest that hamsters provide a good model for investigation of hormonal and nutritional regulation of glucose and lipid metabolism.

Original languageEnglish (US)
Pages (from-to)208-213
Number of pages6
JournalJournal of Laboratory and Clinical Medicine
Volume128
Issue number2
StatePublished - Aug 1996

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Dietary Carbohydrates
Mesocricetus
Fructose
Lipid Metabolism
Sucrose
Glucose
Cricetinae
Control Groups
Insulin Resistance
Hypertriglyceridemia
Nonesterified Fatty Acids
Insulin
Plasmas
Triglycerides
Liver
Rats
Fasting
Weights and Measures
Abdominal Obesity
Glucose Tolerance Test

ASJC Scopus subject areas

  • Medicine(all)
  • Pathology and Forensic Medicine

Cite this

Effects of dietary carbohydrates on glucose and lipid metabolism in golden Syrian hamsters. / Karakas, Siddika E; Vriend, Heidi; Almario, Rogelio; Chow, Lap Chi; Goodman, Michael N.

In: Journal of Laboratory and Clinical Medicine, Vol. 128, No. 2, 08.1996, p. 208-213.

Research output: Contribution to journalArticle

Karakas, Siddika E ; Vriend, Heidi ; Almario, Rogelio ; Chow, Lap Chi ; Goodman, Michael N. / Effects of dietary carbohydrates on glucose and lipid metabolism in golden Syrian hamsters. In: Journal of Laboratory and Clinical Medicine. 1996 ; Vol. 128, No. 2. pp. 208-213.
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abstract = "Frequent coexistence of insulin resistance, central obesity, and hypertriglyceridemia in the same individual suggests an underlying common pathogenesis. Insulin resistance and hypertriglyceridemia can be induced by carbohydrate feeding in rats. Golden Syrian hamsters are believed to be resistant to the metabolic effects of dietary carbohydrates. We investigated the effects of diets containing 60{\%} fructose or sucrose on glucose and lipid metabolism in hamsters, both in the fasting state and during an intravenous glucose tolerance test. Fructose caused obesity (weight after treatment: 131 ± 7 gm in the control group, 155 ± 5 gm in the fructose group, 136 ± 7 gm in sucrose group, p < 0.04). Fructose also reduced glucose disappearance rate (K(G): 2.69{\%} ± 0.39{\%} in the control group, 1.45{\%} ± 0.18{\%} in the fructose group, p < 0.02). Sucrose caused a marginal decrease in glucose disappearance (K(G): 1.93{\%} ± 0.21{\%}, p = 0.08 vs the control group). Only fructose feeding increased fasting plasma nonesterified fatty acids (0.645 ± 0.087 mEq/L in the control group, 1.035 ± 0.083 mEq/L in the fructose group, 0.606 ± 0.061 mEq/L in the sucrose group, p < 0.002), plasma triglycerides (84 ± 6 mg/dl in the control group, 270 ± 65 mg/dl in the fructose group, 94 ± 16 mg/dl in the sucrose group, p < 0.0002), and liver triglycerides (1.88 ± 0.38 mg/gm liver weight in the control group, 2.35 ± 0.24 mg/gm in the fructose group, 1.41 ± 0.13 mg/gm in the sucrose group, p < 0.04). Previous studies in the rat have suggested that dietary carbohydrates induce insulin resistance by increasing plasma nonesterified fatty acids and triglycerides, which are preferentially used by the muscles. The present report shows that sucrose also can cause some decrease in glucose disappearance in the hamster without causing hypertriglyceridemia or increasing plasma nonesterified fatty acids. Thus other mechanisms may also contribute to the insulin resistance in the hamster. These findings suggest that hamsters provide a good model for investigation of hormonal and nutritional regulation of glucose and lipid metabolism.",
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