Hormonal
Insulin resistance in NAFLD creates a paradoxical state where insulin fails to suppress hepatic glucose production (causing hyperglycemia) while simultaneously stimulating de novo lipogenesis (causing hepatic steatosis).
If you have fatty liver, your body's insulin signaling is broken in a specific way: your liver ignores insulin's command to stop making sugar, but it still obeys insulin's command to make fat. This means standard 'low insulin' strategies might not address the root cause if they don't improve the specific insulin signaling pathway (PI3K-AKT) in the liver. Focus on improving overall insulin sensitivity through lifestyle changes rather than just avoiding insulin-producing foods.
This paradox in hepatic insulin resistance is that insulin fails to suppress hepatic glucose production, yet it continues to stimulate lipogenesis, resulting in hyperglycemia, hyperlipidemia, hepatic steatosis, and type 2 diabetes.
Why this rating
The paper is a comprehensive review citing multiple human cohort studies, genetic polymorphisms, and mouse models.
Source
Homeostasis of Glucose and Lipid in Non-Alcoholic Fatty Liver Disease
Hsu‐Wen Chao et al. · International Journal of Molecular Sciences · 2019
DOI 10.3390/ijms20020298
More from this paper
- Excessive dietary intake of carbohydrates, particularly fructose and sucrose, drives hepatic de novo lipogenesis through the activation of the transcription factor ChREBP, contributing to NAFLD progression.Good
- Circadian misalignment, such as night-shift work or irregular eating patterns, impairs hepatic metabolic function and increases the risk of developing NAFLD and insulin resistance.Good
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