The role of visceral and subcutaneous adipose tissue fatty acid composition in liver pathophysiology associated with NAFLD

Biochemical and Physiological Parameters in Rats Fed with High-Fat Diet: The Protective Effect of Chronic Treatment with Purple Grape Juice (Bordo Variety)

“…It also was previously reported that a HFD induced the acceleration of replication of preadipocytes in primary cultures, stimulating a greater expansion of retroperitoneal fat, and inducing the expansion of adipose tissue mass [49]. This result can be harmful to individuals, since increased visceral adiposity is a risk factor for metabolic disorders such as dyslipidemia, diabetes (type 2), inflammation, and fatty liver disease [50,51]. Of note, intake of saturated fat, even without changing body weight, induces insulin resistance, hyperinsulinemia, and visceral adiposity [52,53].…”

Increased hepatic fatty acid polyunsaturation precedes ectopic lipid deposition in the liver in adaptation to high-fat diets in mice

“…This selective accumulation of PUFA in the liver, under conditions of lipid abundance, contributes to curtail intrahepatic SFA levels, thereby limiting SFA-induced lipotoxicity [41]. This mechanism is clearly illustrated by the greater accumulation of lipids in the liver in rats fed a PUFA-rich diet versus rats fed an SFA-rich diet, and the presence of liver damage in the latter but not the former conditions [6]. Reduced MUFA index is consistent with an HFD-induced decrease of stearoyl-CoA desaturase 1 (SCD-1) activity, converting SFA 16:0 and 18:0 to MUFA 16:1 and 18:1 [39,42,43].…”

“…High-fat diet (HFD) feeding is a widely used experimental model to study obesity and its associated metabolic complications. It has been established that prolonged exposure to an HFD not only causes obesity but also compromises liver and adipose tissue physiology, and perturbs beta-cell function [3][4][5][6].…”

“…Not only the amount of fat in the diet but also its qualitative FA composition influences the extent of hepatic FA uptake, hepatic FA accumulation, and ensuing metabolic defects. It has been shown that diets rich in saturated FA (SFA) cause greater metabolic damage than those rich in monounsaturated FA (MUFA) or polyunsaturated FA (PUFA) [6,20,21]. Although the unsaturation features of FA in hepatic triglycerides were shown to mirror those of the diet after long-term exposure in rats [21], tracer methods found that dietary fat is not the major source of hepatic lipids during exogenous lipid delivery [22][23][24].…”

The long-Term Effect of Juvenile Stressor Exposure and Access to Palatable Food: Alterations in Dopamine and Ghrelin Signalling

“…In addition, there was an increase in visceral fat pad however this did not reach significance for previously stressed rats fed on a palatable diet. This is in line with the common findings that have shown that access to a densely caloric diet can lead to increased adipose accumulation (Gentile et al, 2015). In addition, access to a high fat and/or high carbohydrate diet led to heavier mesenteric and subcutaneous fat pad when compared to animals given chow only (Foster et al, 2009;Pecoraro et al, 2004).…”