High-fat feeding induces increased lipid oxidation capacity in skeletal muscle of both diabetic and control rats, though the adaptation is delayed and accompanied by heightened inflammation in the diabetic strain.
Answers are grounded in this paper and cite their sources.
May highlight diabetes gene targets in rat muscle; leaves open human translation.
In the present report, we examined the responses of diabetic Goto-Kakizaki (GK) rats and control Wistar-Kyoto (WKY) rats fed either a standard chow or high-fat diet (HFD) from weaning to 20 weeks of age. This comparison included gene expression profiling of skeletal muscle using Affymetrix gene array chips. The expression profiling is interpreted within the context of a wide array of physiological measurements. Genes whose expressions are different between the 2 strains regardless of diet, as well as genes that differ between strains only with HFD, were identified. In addition, genes that were regulated by diet in 1 or both strains were identified. The results suggest that both strains respond to HFD by an increased capacity to oxidize lipid fuels in the musculature but that this adaptation occurs more rapidly in WKY rats. The results also demonstrated an impaired cytokine signalling and heightened inflammatory status in the GK rats.
No takes yet. Share an insight, caveat, or question.
Nie et al. (2017) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: