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Liver Update: Intestinal gluconeogenesis prevents obesity-linked liver steatosis and non-alcoholic fatty liver disease
Hepatic steatosis with obesity may lead to non-alcoholic fatty liver disease (NAFLD) and associated complications like cirrhosis or cancer. Intestinal gluconeogenesis (IGN) can cause metabolic benefits of specific macronutrients like protein or soluble fibre, via the initiation of a gut-brain nervous signal triggering brain-dependent regulations of peripheral metabolism.
A study investigated the effects of IGN on liver metabolism, independently of its initiation by the given macronutrients.
Specific effects of IGN on hepatic metabolism was studied on two transgenic mouse lines: one is knocked down for and the other overexpresses glucose-6-phosphatase, the key enzyme of endogenous glucose production, specifically in the intestine.
The following observations were made-
- Mice with a genetic overexpression of IGN are distinctly protected from hepatic steatosis development and NAFLD initiation, on a hypercaloric diet.
- The protection may be due to the alleviation of de novo lipogenesis and lipid import, rendering benefits in inflammation and fibrosis and linked to the autonomous nervous system.
- However, mice with genetic suppression of IGN immediately showed increased hepatic triglyceride storage associated with the activated lipogenesis pathway, on a standard starch-enriched diet.
- It was corrected by portal glucose infusion imitating IGN.
It was thus concluded that IGN has the potential to prevent hepatic steatosis and its progress to NAFLD.
Source: Gut 2020;69:2193-2202.