Published online Nov 15, 2016. doi: 10.4239/wjd.v7.i19.534
Peer-review started: June 28, 2016
First decision: August 5, 2016
Revised: August 18, 2016
Accepted: September 7, 2016
Article in press: September 9, 2016
Published online: November 15, 2016
Processing time: 137 Days and 14.6 Hours
To study the effects of linagliptin on the structural signs of non-alcoholic fatty liver disease (NAFLD) in db/db mice.
Male diabetic db/db mice (BKS.Cg-Dock7m+/+Leprdb/J) aged 10 wk received the dipeptidyl peptidase 4 (DPP4) inhibitor linagliptin (10 mg/kg) or saline as a placebo once per day by gavage for 8 wk. Intact db/db mice served as controls. Structural changes in the liver were analyzed from light and electron microscopic images of sections from intact, placebo-treated and linagliptin-treated animals. We estimated the changes in hepatocytes, sinusoidal cells, liver microvasculature and lymphatic roots. Hepatic staining for lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1) was assessed by immunohistochemistry.
In 18-wk-old diabetic mice, liver steatosis (predominantly microvesicular and mediovesicular steatosis) was accompanied by dilation of the roots of the lymphatic system, interlobular blood vessels and bile canaliculi. Compared to saline-treated mice, linagliptin-treated mice exhibited a reduction in the mean numeral densities of hepatocytes with lipid droplets (92.4% ± 1.7% vs 64.9% ± 5.8% per field of view, P = 0.0002) and a lower proportion of hepatocytes with a high density of lipid droplets (20.7% ± 3.6% vs 50.4% ± 3.1%, P = 0.0007). We observed heterogeneous hepatocytes and relatively preserved cell structures in the linagliptin group. Dilation of blood and lymphatic vessels, as well as ultrastructural changes in the hepatocyte endoplasmic reticulum and mitochondria, were alleviated by linagliptin treatment. In intact and placebo-treated mice, immunohistochemical staining for LYVE-1 was observed in the endothelial cells of interlobular lymphatic vessels and on the membranes of some endothelial sinusoidal cells. We observed an enlarged LYVE-1 reaction area in linagliptin-treated mice compared to intact and placebo-treated mice. The improvement in the structural parameters of the liver in linagliptin-treated mice was independent to changes in the plasma glucose levels.
The DPP4 inhibitor linagliptin alleviates liver steatosis and structural changes in the hepatic microvasculature and lymphatic roots in a model of NAFLD in diabetic db/db mice.
Core tip: Dipeptidyl peptidase 4 (DPP4) inhibitors are a relatively new class of hypoglycemic agents with multiple pleiotropic effects. In this study, we demonstrated that the DPP4 inhibitor linagliptin alleviates liver steatosis and diminishes structural changes in hepatic non-parenchymal compartments in db/db diabetic mice. The mechanism of the beneficial effect of linagliptin seems to be glucose-independent as no obvious hypoglycemic activity of the agent was observed in this model. The results of the study provide further evidence that linagliptin could be a promising agent for the treatment of non-alcoholic fatty liver disease in subjects with type 2 diabetes.