The liver is at the center of Metabolic Syndrome (Yki-Järvinen, Hannele. Nutritional Modulation of Non-Alcoholic Fatty Liver Disease and Insulin Resistance. Nutrients 7.11 (2015): 9127–9138. PMC. Web. 22 May 2018.) states the reason why this is relevant.
If the liver is fatty due to causes of insulin resistance such as obesity and physical inactivity, it overproduces glucose and triglycerides leading to hyperinsulinemia and a low high-density lipoprotein (HDL) cholesterol concentration.
How do you tell if you have a Fatty Liver?
Trouble is blood tests don’t tell you most of the time.
NAFLD is usually asymptomatic and most patients have normal transaminases (ALT <30–40 U/L for men and <20–30 U/L for women)
See also (J Res Med Sci. 2016; 21: 53. The effects of low carbohydrate diets on liver function tests in nonalcoholic fatty liver disease: A systematic review and meta-analysis of clinical trials. Fahimeh Haghighatdoost, et.al.).
… we conducted a meta-analysis of clinical trial data to summarize the effects of LCDs on liver function tests in NAFLD.
Low Carb Diet consumption in subjects with NAFLD led to a significant reduction in IHLC, but did not significantly affect the concentration of liver enzymes.
Metabolic Syndrome Development
Pathophysiology of “Metabolic NAFLD”, which causes and consequences resemble those of the insulin resistance/metabolic syndrome (MetS).
Overeating and physical inactivity predispose to both conditions.
Excess glucose, fructose and amino acids are converted to triglyceride (TG) in the liver via de novo lipogenesis (DNL), which pathway is increased in NAFLD.
Alterations in gut microbiota in obesity increase gut permeability to bacterial components such as lipopolysaccharide (LPS), which may contribute to inflammation in both adipose tissue and the liver.
Overeating leads to adipose tissue expansion, hypoxia, increased fibrosis and cell death. Dead adipocytes are surrounded by macrophages, which produce cytokines such as tumor-necrosis alpha and chemokines such as monocyte chemoattractant protein-1. This impairs the ability of insulin to inhibit lipolysis i.e., inhibit release of free fatty acids (FFA) and leads to deficiency of the insulin-sensitizing cytokine adiponectin. The latter two changes promote synthesis of intrahepatocellular TG.
The ability of insulin to suppress glucose and VLDL production is impaired resulting in mild hyperglycemia and hyperinsulinemia, hypertriglyceridemia (TG↑) and a low HDL cholesterol concentration (HDL chol↓).
The fatty liver also overproduces many other factors such as the liver enzymes alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyltransferase (GGT), C-reactive protein (CRP) and coagulation factors.
This paragraph really summarizes it well:
Hypocaloric, especially low carbohydrate ketogenic diets rapidly decrease liver fat content and associated metabolic abnormalities. However, any type of caloric restriction seems effective long-term. Isocaloric diets containing 16%–23% fat and 57%–65% carbohydrate lower liver fat compared to diets with 43%–55% fat and 27%–38% carbohydrate. Diets rich in saturated (SFA) as compared to monounsaturated (MUFA) or polyunsaturated (PUFA) fatty acids appear particularly harmful as they increase both liver fat and insulin resistance. Overfeeding either saturated fat or carbohydrate increases liver fat content.
Low carb works much better once again.