Session: SAT 723-745-Lipids: Fatty Liver Disease & Lipodystrophies
Poster Board SAT-725
Methods: Twenty-four weeks old, 199-240 grams, 24 adult female Sprague-Dawley rats were randomly separated into two groups: control group (n=6) was fed with standard rat diet; the remaining rats (n=18) were fed with a high-fat diet (HFD) to induce NAFLD. After 12 weeks, rats fed with a HFD were randomly separated into 2 groups: (i) HFD-only group (n=8) was fed with a HFD for an additional 4 weeks, (ii) HFD-Sitagliptin group (n=10) received sitagliptin (3 mg/kg) for 4 weeks in addition to HFD. At the end of the study (16thweek), blood samples were drawn from all rats to determine serum glucose, triglyceride, cholesterol, alanine aminotransferase (ALT), and plasma insulin levels. Insulin resistance was determined using the HOMA-IR index. Histopathologic evaluation of liver samples were undertaken.
Results: HFD-Sitagliptin group had significantly lower serum glucose (140.8±18.8 vs. 224.7±20.6 mg/dl, p<0.001), plasma insulin (15.8±4.4 vs. 28.0±5.9 µIU/L, p<0.001), HOMA-IR index (4.9±1.8 vs. 15.9±2.3, p<0.001), serum triglyceride (199.0±108.7 vs. 468.0±370.7 mg/dl, p<0.001) and cholesterol (82.0±26.7 vs. 90.5±7.0, p<0.001) values compared to HFD-only group. Hepatic steatosis was significantly less (mean score: 1 vs 2; p<0.001) in HFD-Sitagliptin group compared to HFD-only group while there was no difference in hepatic inflammation (p=0.057) and ALT levels (p= 0.232).
Conclusion: Sitagliptin improves hepatic steatosis in rats. The clinical potential of sitagliptin as an agent for the treatment of NAFLD needs further research.
Nothing to Disclose: SB, CK, GY, NC, MA, FT
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