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. 2023 Oct 2;12:RP88049. doi: 10.7554/eLife.88049

Figure 4. ADGAT DKO mice are resistant to diet-induced obesity and glucose intolerance.

(A) ADGAT DKO mice stay lean on a high-fat diet (HFD). Representative photographs of male mice fed on HFD for 12 weeks. (B) Both male and female ADGAT DKO mice gained ~40% less body weight than control mice. Body weights of mice fed on a chow-diet or HFD (n=15 for males, n=12 for females). (C) ADGAT DKO mice had decreased fat mass on HFD feeding. Dual-energy X-ray absorptiometry (DEXA) analysis of lean mass and fat mass of HFD fed male mice (n=10). (D) ADGAT DKO male mice had normal food intake during HFD feeding (n=5). (E and F) ADGAT DKO mice had increased energy expenditures. Energy expenditure and respiratory quotient on HFD-fed male mice measured by indirect calorimetry. Values were normalized to lean mass (n=4). (G and H) ADGAT DKO mice were protected from HFD-induced glucose intolerance and insulin resistance. Glucose- and insulin-tolerance tests were performed on HFD-fed (for 9 or 10 weeks, respectively) male mice (n=10). AUC, area under the curve. (I) Liver weights and triglyceride levels were moderately increased in HFD-fed ADGAT DKO male mice (n=6). Data are presented as mean ± SD. *p<0.05, **p<0.01, ***p<0.001.

Figure 4.

Figure 4—figure supplement 1. ADGAT DKO mice gradually activate an alternative mechanism to synthesize triglycerides.

Figure 4—figure supplement 1.

(A) Lipid droplets (LDs) isolated from inguinal white adipose tissue (iWAT) of mice fed a high-fat diet (HFD). (B) Blood glucose levels in HFD-fed male mice (n=8). (C) Insulin levels in HFD-fed male mice (n=8). (D) Relative mRNA levels in livers of HFD mice (n=6). Data are presented as mean ± SD. *p<0.05, **p<0.01, ***p<0.001.