Increased hepatic Akt phosphorylation alleviated glucose intolerance and improved liver function 
in leptin-deficient mice

Tomer Adar; Meir Mizrahi; Yoav Lichtenstein; Yehudit Shabat; Rizan Sakhnini; Lida Zolotarov; Naim Shehadeh; Yaron Ilan

doi:10.5114/ceh.2023.127849

eISSN: 2449-8238
ISSN: 2392-1099

Clinical and Experimental Hepatology

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abstract:

Original paper

Increased hepatic Akt phosphorylation alleviated glucose intolerance and improved liver function in leptin-deficient mice

Tomer Adar

¹

,

Meir Mizrahi

¹

,

Yoav Lichtenstein

¹

,

Yehudit Shabat

¹

,

Rizan Sakhnini

²

,

Lida Zolotarov

¹

,

Naim Shehadeh

²

,

Yaron Ilan

¹

Department of Medicine, Hadassah Medical Center and Faculty of Medicine, Hebrew University, Jerusalem, Israel
Rambam Medical Center, Haifa, Israel

Clin Exp HEPATOL 2023; 9, 2: 164-171

DOI: https://doi.org/10.5114/ceh.2023.127849

Online publish date: 2023/06/23

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Aim of the study:
Akt is involved in upregulating the insulin-signaling pathways essential for maintaining glucose metabolism. Glycosphingolipids are involved in the pathogenesis of glucose intolerance and associated target organ injury. On the other hand, oral administration of b-glucosylceramide (GC) has been shown to alleviate insulin resistance. The present study aimed to determine the effects of oral administration of insulin and GC, separately and in combination, on Akt expression and the subsequent effect on metabolic syndrome characteristics in leptin-deficient mice.

Material and methods:
Four groups of leptin-deficient ob/ob mice were orally administered for four weeks: vehicle, GC, short-acting insulin, and GC combined with insulin. Mice were followed for hepatic Akt expression and changes in tumor necrosis factor a (TNF-a) level, hyperlipidemia, and liver damage.

Results:
Four groups of leptin-deficient ob/ob mice were orally administered for four weeks: vehicle, GC, short-acting insulin, and GC combined with insulin. Mice were followed for hepatic Akt expression and changes in tumor necrosis factor a (TNF-a) level, hyperlipidemia, and liver damage.

Conclusions:
These data established the potential use of oral insulin administration with glycosphingolipids to alleviate glucose intolerance and associated liver damage and hyperlipidemia via increased Akt expression in the liver. The data support targeting Akt as a potent therapeutic target for metabolic syndrome.

keywords:

Increased hepatic Akt phosphorylation alleviated glucose intolerance and improved liver function in leptin-deficient mice

Tomer Adar 1 , Meir Mizrahi 1 , Yoav Lichtenstein 1 , Yehudit Shabat 1 , Rizan Sakhnini 2 , Lida Zolotarov 1 , Naim Shehadeh 2 , Yaron Ilan 1

AKT, NAFLD, diabetes, steatosis, TNF-a

Tomer Adar

¹

,

Meir Mizrahi

¹

,

Yoav Lichtenstein

¹

,

Yehudit Shabat

¹

,

Rizan Sakhnini

²

,

Lida Zolotarov

¹

,

Naim Shehadeh

²

,

Yaron Ilan

¹