Skeletal muscle respiratory capacity is enhanced in rats consuming an obesogenic western diet

Erin Stephenson, Donny M. Camera, Trisha A. Jenkins, Sepideh Kosari, Jong Sam Lee, John A. Hawley, Nigel K. Stepto

Research output: Contribution to journalArticle

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Abstract

Obesity-induced lipid over-supply promotes skeletal muscle mitochondrial biogenesis. Previous investigations have utilized extreme high-fat diets (HFD) to induce such mitochondrial perturbations despite their disparity from human obesogenic diets. Here, we evaluate the effects of Western diet (WD)-induced obesity on skeletal muscle mitochondrial function. Long-Evans rats were given ad libitum access to either a WD [40% energy (E) from fat, 17% protein, and 43% carbohydrate (30% sucrose); n = 12] or a control diet (CON; 16% of E from fat, 21% protein, and 63% carbohydrate; n = 12) for 12 wk. Rats fed the WD consumed 23% more E than CON (P = 0.0001), which was associated with greater increases in body mass (23%, P = 0.0002) and adiposity (17%, P = 0.03). There were no differences in fasting blood glucose concentration or glucose tolerance between diets, although fasting insulin was increased by 40% (P = 0.007). Fasting serum triglycerides were also elevated in WD (86%, P = 0.001). The maximal capacity of the electron transfer system was greater following WD (37%, P = 0.02), as were the maximal activities of several mitochondrial enzymes (citrate synthase, (β-hydroxyacyl-CoA dehydrogenase, carnitine palmitoyltransferase). Protein expression of citrate synthase, UCP3, and individual respiratory complexes was greater after WD (P < 0.05) despite no differences in the expression of peroxisome proliferator-activated receptor (PPAR)α, PPARδ, or PPARγ coactivator-1 mRNA or protein abundance. We conclude that the respiratory capacity of skeletal muscle is enhanced in response to the excess energy supplied by a WD. This is likely due to an increase in mitochondrial density, which at least in the short term, and in the absence of increased energy demand, may protect the tissue from lipid-induced impairments in glycemic control.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume302
Issue number12
DOIs
StatePublished - Jun 15 2012

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Skeletal Muscle
Peroxisome Proliferator-Activated Receptors
Citrate (si)-Synthase
Fasting
Diet
Proteins
Obesity
Fats
Carbohydrates
Carnitine O-Palmitoyltransferase
Lipids
Long Evans Rats
Adiposity
High Fat Diet
Organelle Biogenesis
Coenzyme A
Western Diet
Sucrose
Blood Glucose
Oxidoreductases

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)
  • Endocrinology, Diabetes and Metabolism

Cite this

Skeletal muscle respiratory capacity is enhanced in rats consuming an obesogenic western diet. / Stephenson, Erin; Camera, Donny M.; Jenkins, Trisha A.; Kosari, Sepideh; Lee, Jong Sam; Hawley, John A.; Stepto, Nigel K.

In: American Journal of Physiology - Endocrinology and Metabolism, Vol. 302, No. 12, 15.06.2012.

Research output: Contribution to journalArticle

Stephenson, Erin ; Camera, Donny M. ; Jenkins, Trisha A. ; Kosari, Sepideh ; Lee, Jong Sam ; Hawley, John A. ; Stepto, Nigel K. / Skeletal muscle respiratory capacity is enhanced in rats consuming an obesogenic western diet. In: American Journal of Physiology - Endocrinology and Metabolism. 2012 ; Vol. 302, No. 12.
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abstract = "Obesity-induced lipid over-supply promotes skeletal muscle mitochondrial biogenesis. Previous investigations have utilized extreme high-fat diets (HFD) to induce such mitochondrial perturbations despite their disparity from human obesogenic diets. Here, we evaluate the effects of Western diet (WD)-induced obesity on skeletal muscle mitochondrial function. Long-Evans rats were given ad libitum access to either a WD [40{\%} energy (E) from fat, 17{\%} protein, and 43{\%} carbohydrate (30{\%} sucrose); n = 12] or a control diet (CON; 16{\%} of E from fat, 21{\%} protein, and 63{\%} carbohydrate; n = 12) for 12 wk. Rats fed the WD consumed 23{\%} more E than CON (P = 0.0001), which was associated with greater increases in body mass (23{\%}, P = 0.0002) and adiposity (17{\%}, P = 0.03). There were no differences in fasting blood glucose concentration or glucose tolerance between diets, although fasting insulin was increased by 40{\%} (P = 0.007). Fasting serum triglycerides were also elevated in WD (86{\%}, P = 0.001). The maximal capacity of the electron transfer system was greater following WD (37{\%}, P = 0.02), as were the maximal activities of several mitochondrial enzymes (citrate synthase, (β-hydroxyacyl-CoA dehydrogenase, carnitine palmitoyltransferase). Protein expression of citrate synthase, UCP3, and individual respiratory complexes was greater after WD (P < 0.05) despite no differences in the expression of peroxisome proliferator-activated receptor (PPAR)α, PPARδ, or PPARγ coactivator-1 mRNA or protein abundance. We conclude that the respiratory capacity of skeletal muscle is enhanced in response to the excess energy supplied by a WD. This is likely due to an increase in mitochondrial density, which at least in the short term, and in the absence of increased energy demand, may protect the tissue from lipid-induced impairments in glycemic control.",
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AU - Lee, Jong Sam

AU - Hawley, John A.

AU - Stepto, Nigel K.

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