Effect of visceral fat composition on its lipolysis and associated inflammatory response. (A) Gross appearance of the FN in SFA-fed (top) and UFA-fed mice with pancreatitis. (B1) PNLIP, IKB-, and -tubulin (-Tub) amounts on Western blotting (B2) in the fat pads of SFA-or UFA-fed control (Con) mice or those with CER pancreatitis (CER). Cytokine mRNA levels in fat pads (C1) shown as an increase over control levels or serum levels of IL-6 (C2), MCP-1 (C3), or TNF- (C4) in control mice or those with CER pancreatitis after they had been fed with UFA-or SFA-enriched diets. Serum NEFA showing OA (D1), LA (D2), total serum UFA (C3), total serum NEFA (D4), PA (D5), palmitoleic acid (D6), total serum SFA (D7), and serum SFA as a percentage of total NEFA (D8) in control mice or those with CER pancreatitis after they had been fed with UFA-or SFA-enriched diets. Photo credit: Krutika Patel, Mayo Clinic, AZ.

Effect of visceral fat composition on its lipolysis and associated inflammatory response. (A) Gross appearance of the FN in SFA-fed (top) and UFA-fed mice with pancreatitis. (B1) PNLIP, IKB-, and -tubulin (-Tub) amounts on Western blotting (B2) in the fat pads of SFA-or UFA-fed control (Con) mice or those with CER pancreatitis (CER). Cytokine mRNA levels in fat pads (C1) shown as an increase over control levels or serum levels of IL-6 (C2), MCP-1 (C3), or TNF- (C4) in control mice or those with CER pancreatitis after they had been fed with UFA-or SFA-enriched diets. Serum NEFA showing OA (D1), LA (D2), total serum UFA (C3), total serum NEFA (D4), PA (D5), palmitoleic acid (D6), total serum SFA (D7), and serum SFA as a percentage of total NEFA (D8) in control mice or those with CER pancreatitis after they had been fed with UFA-or SFA-enriched diets. Photo credit: Krutika Patel, Mayo Clinic, AZ.

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Obesity sometimes seems protective in disease. This obesity paradox is predominantly described in reports from the Western Hemisphere during acute illnesses. Since adipose triglyceride composition corresponds to long-term dietary patterns, we performed a meta-analysis modeling the effect of obesity on severity of acute pancreatitis, in the context...

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... 12À14 This process, if uncontrolled, generates an overwhelmed amount of nonesterified fatty acids (NEFAs), which in turn aggravate the damage to pancreatic acinar cells and even lead to organ failure. 12,13,15 The liver serves as a metabolic hub responsible for maintaining the homeostasis of fatty acids, glucose, and amino acids. 16 Fatty acid b-oxidation (FAO) is a major catabolic process that degrades long-chain (LC) acyl-CoA to acetyl-CoA, 17 which then enters the tricarboxylic acid (TCA) cycle or ketogenesis process for energy production. ...
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... Stratified by BMI, mortality was lowest in individuals with normal weight (4.5%) and highest in class III obese (7%) ( Table 1). After adjusting for covariates (including AAST grade), overweight, class I, and class II (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33) 0.157 20.5 (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29) 21 (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29) 0.024 21 (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29) 0.733 20 (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29) 0.739 21 (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29) World J Surg obesity were not protective against mortality, whereas underweight and class III obesity were associated with increased odds of mortality (Table 3). ...
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... Emerging evidence has con rmed that aberrant metabolic reprogramming, especially glycolysis [3,4], mitochondrial oxidative phosphorylation [5,6], cholesterol metabolic pathways [7], and fatty acid metabolism [8], contributed to the occurrence of many diseases, including cancers and in ammation [9]. ...
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