Holmstroem 2013 Metabolism

From Bioblast
Revision as of 14:51, 27 April 2015 by Bader Helga (talk | contribs)
(diff) ← Older revision | Latest revision (diff) | Newer revision β†’ (diff)
Publications in the MiPMap
HolmstrΓΆm MH, Tom RZ, BjΓΆrnholm M, Garcia-Roves PM, Zierath JR (2013) Effect of leptin treatment on mitochondrial function in obese leptin-deficient ob/ob mice. Metabolism 62:1258-67.

Β» PMID: 23664724

Holmstroem MH, Tom RZ, Bjoernholm M, Garcia-Roves PM, Zierath JR (2013) Metabolism

Abstract: Leptin stimulates peripheral lipid oxidation, but the influence on mitochondrial function is partly unknown. We investigated tissue-specific mitochondrial function in leptin-deficient obese C57BL/6J-ob/ob mice compared to lean littermates following leptin treatment.

Lean and obese ob/ob mice were treated with saline or leptin for 5days. At day six, liver, extensor digitorum longus (EDL) and soleus muscle were dissected and mitochondrial respiration analyzed in freshly dissected tissues. Expression of key proteins in the regulation of mitochondrial function was determined.

In liver, mitochondrial respiration was reduced in ob/ob mice compared to lean mice. Expression of mitochondrial transcription factor A (TFAM) was decreased in ob/ob mice, but increased with leptin treatment. In glycolytic EDL muscle, mitochondrial respiration was increased in ob/ob mice. Protein markers of complex II, IV and ATP synthase were increased in EDL muscle from both saline- and leptin-treated ob/ob mice. TFAM protein abundance was decreased, while dynamin-1-like protein was increased in EDL muscle from saline-treated ob/ob mice and restored by leptin treatment. In oxidative soleus muscle, mitochondrial respiration and electron transport system protein abundance were unchanged, while TFAM was reduced in ob/ob mice.

In conclusion, leptin-deficient ob/ob mice display tissue-specific mitochondrial adaptations under basal conditions and in response to leptin treatment. Mitochondrial respiration was decreased in liver, increased in glycolytic muscle and unaltered in oxidative muscle from ob/ob mice. Insight into the tissue-specific regulation of mitochondrial function in response to energy supply and demand may provide new opportunities for the treatment of insulin resistance. β€’ Keywords: Leptin, Mitochondria, Skeletal Muscle Metabolism, Liver, Therapy Intervention

β€’ O2k-Network Lab: ES Barcelona Garcia-Roves PM, SE Stockholm Morein T

Labels: MiParea: Respiration, Genetic knockout;overexpression  Pathology: Diabetes, Obesity 

Organism: Mouse  Tissue;cell: Skeletal muscle, Liver  Preparation: Permeabilized tissue 

HRR: Oxygraph-2k 

Cookies help us deliver our services. By using our services, you agree to our use of cookies.