Apr 2, 2020

Adipose depot-specific upregulation of Ucp1 or mitochondrial oxidative complex proteins are early consequences of genetic insulin reduction in mice

BioRxiv : the Preprint Server for Biology
J. D. BotezelliJames D Johnson

Abstract

Hyperinsulinemia plays a causal role in adiposity tissue expansion. We have previously shown that mice with reduced insulin gene dosage have increased energy expenditure, but the tissue-specific molecular mechanisms involved in the effects of abrogated hyperinsulinemia have remained unclear. Herein we investigated the effects of genetically reducing insulin production on the abundance of oxidative mitochondrial complex proteins in liver, skeletal muscle, white adipose tissue and brown adipose tissue. To suppress insulin levels, we manipulated Ins1 gene dosage in mice lacking both Ins2 alleles to prevent compensation. Male Ins1+/+ or Ins1+/- littermates were fed either a low-fat diet (LFD) or a high-fat diet (HFD) for 4 weeks, starting at 8 weeks of age. As expected, HFD increased fasting hyperinsulinemia, and Ins1+/- mice had significantly lower circulating insulin compared with Ins1+/+ littermate controls. Fasting glucose and body weight were not significantly different between genotypes at any time over the 4 weeks of study. In liver and skeletal muscle, protein abundances reflecting complex I (Ndufb8), II (Sdhb), III (Uqcrc2), and V (Atp5a1) were not consistently different between groups. In mesenteric white adipose tissue, ...Continue Reading

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Mentioned in this Paper

Peptide Hydrolases
Nucleic Acid Sequencing
Endopeptidases
Cleaved Cell
Sequencing
Tandem
Polymers
Pore
CGP-30694
probe gene fragment

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