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Homozygous glucagon-GFP knock-in mice ( Gcg    gfp/gfp  ) lack proglucagon derived-peptides including glucagon and GLP-1, and are normoglycemic. We have previously shown that  Gcg    gfp/gfp   show improved glucose tolerance with enhanced insulin secretion. Here, we studied glucose and energy metabolism in  Gcg    gfp/gfp   mice fed a high-fat diet (HFD). Male  Gcg    gfp/gfp   and  Gcg    gfp/+   mice were fed either a normal chow diet (NCD) or an HFD for 15–20 weeks. Regardless of the genotype, mice on an HFD showed glucose intolerance, and  Gcg    gfp/gfp   mice on HFD exhibited impaired insulin secretion whereas  Gcg    gfp/+   mice on HFD exhibited increased insulin secretion. A compensatory increase in β-cell mass was observed in  Gcg    gfp/+  mice on HFD, but not in  Gcg    gfp/gfp   mice on the same diet. Weight gain was significantly lower in  Gcg    gfp/gfp   mice than in  Gcg    gfp/+  mice. Oxygen consumption was enhanced in  Gcg    gfp/gfp   mice compared to  Gcg    gfp/+   mice on an HFD. HFD feeding significantly increased uncoupling protein 1 mRNA expression in brown adipose and inguinal white adipose tissues of  Gcg    gfp/gfp   mice, but not of  Gcg    gfp/+  mice. Treatment with the glucagon-like peptide-1 receptor agonist liraglutide (200 mg/kg) improved glucose tolerance in  Gcg    gfp/gfp   mice and insulin content in  Gcg    gfp/gfp   and  Gcg    gfp/+   mice was similar after liraglutide treatment. Our findings demonstrate that  Gcg    gfp/gfp   mice develop diabetes upon HFD-feeding in the absence of proglucagon-derived peptides, although they are resistant to diet-induced obesity.

Mice Deficient in Proglucagon-Derived Peptides Exhibit Glucose Intolerance on a High-Fat Diet but Are Resistant to Obesity