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Atg6 deficiency exacerbates glucose intolerance in mice on high‐fat diet
Author(s) -
Greene Nicholas Perry,
Lira Vitor A,
Yan Zhen
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.869.18
Subject(s) - medicine , endocrinology , basal (medicine) , autophagy , homeostasis , glucose homeostasis , biology , obesity , diabetes mellitus , biochemistry , insulin resistance , apoptosis
Autophagy is critical in clearing damaged organelles (i.e. mitochondria) and aggregate proteins for the maintenance of metabolic homeostasis, and is dependent on the function of autophagy related protein 6 (Atg6). To test the hypothesis that autophagy is required for the maintenance of glucose tolerance under the condition of high‐fat diet (HFD) we subjected Atg6 heterozygous knockout mice (Atg6 +/− ) and wild type (WT) littermates to either normal chow (NC) or 45% HFD beginning at 12wks of age for a period of 8wks. At the conclusion of 8wks HFD, mice were subjected to intraperitoneal glucose tolerance test (GTT, 1.5g glucose/kg body weight) with blood glucose measured before and at 30, 60, and 120min following injection. No difference was seen in GTT between Atg6 +/− and WT mice on NC, while Atg6 +/− mice on HFD demonstrated a 42% greater mean integrated area under the curve than that of WT mice on HFD (2.35 vs. 1.65mg/dL*min*10 4 ) with no difference in body weight between genotypes. These findings demonstrate that deficiency of Atg6 exacerbates HFD‐induced glucose intolerance in mice and provides new insight to the relevance of basal autophagy for the maintenance of whole‐body metabolic homeostasis.