Cited by 618Diet, Metabolism, and DiseaseAdipokines, Inflammation, and Metabolic DiseasesRegulation of Appetite and Obesity

Differential effects of fat and sucrose on the development of obesity and diabetes in C57BL/6J and mice

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Surwit, R.S., Feinglos, M.N., Rodin, J., Sutherland, A., Petro, A.E., Opara, E.C., Kuhn, C.M., Rebuffe-Scrive, M.·1995·Metabolism

Abstract

We have previously demonstrated that the C57BL/6J (B/6J) mouse will develop severe obesity, hyperglycemia, and hyperinsulinemia if weaned onto a high-fat, high-sucrose (HH) diet. In the present study, we compared the effects of fat and sucrose separately and in combination on diabetes- and obesity-prone B/6J and diabetes- and obesity-resistant A/J mice. After 4 months, the feed efficiency ([FE] weight gained divided by calories consumed) did not differ across diets in A/J mice, but B/6J mice showed a significantly increased FE for fat. That is, B/6J mice gained more weight on high-fat diets without consuming more calories than A/J mice. The increase in FE was related to adipocyte hyperplasia in B/6J mice on high-fat diets. Fat-induced obesity in B/6J mice was unrelated to adrenal cortical activity. In the absence of fat, sucrose produced a decreased in FE in both strains. Animals fed a low-fat, high-sucrose (LH) diet were actually leaner than animals fed a high-complex-carbohydrate diet. Fat was also found to be the critical stimulus for hyperglycemia and hyperinsulinemia in B/6J mice. In the absence of fat, sucrose had no effect on plasma glucose or insulin. These data clearly show that across these two strains of mice, genetic differences in the metabolic response to fat are more important in the development of obesity and diabetes than the increased caloric content of a high-fat diet.

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  • The reductions in genes involved in OXPHOS and mitochondrial biogenesis were recapitulated in an animal model of dietary-induced obesity and insulin resistance and were of much greater magnitude in mice compared with man.

    “Additionally, we have shown that the reductions in genes involved in OXPHOS and mitochondrial biogenesis were recapitulated in an animal model of dietary-induced obesity and insulin resistance (32) and were of a much greater magnitude in mice compared with man.”

    From A High-Fat Diet Coordinately Downregulates Genes Required for Mitochondrial Oxidative Phosphorylation in Skeletal Muscle (2005) · cites this paper as [32]

    The Materials and Methods and Discussion (page numbers unavailable) establish a dietary-induced obesity and diabetes model in C57BL/6J mice. The paper does not report reductions in OXPHOS or mitochondrial-biogenesis genes, or compare the magnitude of such reductions in mice and humans. (LLM, conf=0.88)

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Authors
Surwit, R. S., Feinglos, M. N., Rodin, J., Sutherland, A., Petro, A. E., Opara, E. C., Kuhn, C. M., & Rebuffe-Scrive, M.
Affiliations
Duke University (US)
Venue
Metabolism
Publisher
Elsevier BV
Published
1995-05
Volume
44
Issue
5
Pages
645-651
ISSN
0026-0495 (ISSN-L)
OpenAlex
W2153321120
Cited by
618
References
33
Citations by year
2026: 6 · 2025: 9 · 2024: 13 · 2023: 12 · 2022: 16 · 2021: 22 · 2020: 20 · 2019: 15 · 2018: 21 · 2017: 30 · 2016: 27 · 2015: 18 · 2014: 32 · 2013: 45 · 2012: 34
FWCI
5.79
Type
journal article
Language
en
Open access
Locations
  • Metabolism (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Funders
  • American Diabetes Association
  • John D. and Catherine T. MacArthur Foundation
  • National Institutes of Health
  • National Institute of Mental Health (MH 00303)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01-DK24923)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Keywords
high-fat diet, sucrose, obesity, diabetes mellitus, C57BL/6J mice, A/J mice, feed efficiency, adipocyte hyperplasia, hyperglycemia, hyperinsulinemia, genetic susceptibility, adrenal cortex, complex carbohydrates, energy intake
MeSH terms
Adipose Tissue, Analysis of Variance, Animals, Blood Glucose, Body Weight, Energy Intake, Diabetes Mellitus, Dietary Carbohydrates, Dietary Fats, Hyperplasia, Insulin, Male, Mice, Inbred A, Mice, Inbred C57BL, Obesity, Organ Size, Sucrose, Weight Gain, Mice

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