Myostatin null mice respond differently to dietary-induced and genetic obesity

Anna C. Dilger, Michael E. Spurlock, Alan L. Grant, David E. Gerrard

Research output: Contribution to journalArticlepeer-review

Abstract

Our objective was to determine sensitivity of myostatin null (MN) mice to obesity induction by dietary or genetic means. To induce dietary obesity, 3-week-old wild type (WT) and MN mice were fed diets with 60% calories (HF) or 10% calories from fat (LF) for 4 weeks. MN mice did gain body fat on the HF diet but to a lesser extent than WT mice. Body weight and fat content was similar in MN mice fed HF and LF diets. To induce genetic obesity, the MN mutation was incorporated into leptin db/db (DB) mice generating mice homozygous for each mutation (MNDB). Nine-week-old MNDB mice were obese, similar to DB mice. Body weight, body fat content, fat pad weight and adipocyte size were all increased in MNDB mice compared to MN and WT mice and were quite similar to DB mice. However, fasting blood glucose, an indicator of insulin resistance and diabetes, was reduced in MNDB mice compared to DB mice. These results indicate that MN mice gain less body fat than WT on a HF diet, but the MN mutation does not alter fat accumulation caused by DB mutation. Thus, MN mice are not always resistant to obesity development.

Original languageEnglish (US)
Pages (from-to)586-593
Number of pages8
JournalAnimal Science Journal
Volume81
Issue number5
DOIs
StatePublished - Oct 1 2010
Externally publishedYes

Keywords

  • Leptin
  • Mice
  • Muscle
  • Myostatin
  • Obesity

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)

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