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Abstract.: Glycerol is one of the additives which stabilize collagen, as well as globular proteins, against thermally induced denaturation --an effect explained by preferential hydration, i.e. by the formation, in water/glycerol solvents, of a hydration layer whose entropic cost favors the more compact triple-helix native structure against the denatured one, gelatin. Quenching gelatin solutions promotes renaturation which, however, remains incomplete, as the formation of a gel network gives rise to growing topological constraints. So, gelatin gels exhibit glass-like dynamical features such as slow aging of their shear modulus and stretched exponential stress relaxation, the study of which gives us access to the re(de)naturation dynamics of collagen. We show that this dynamics is independent of the bulk solvent viscosity and controlled by a single parameter, the undercooling $ \Delta T$ below the glycerol-concentration-dependent denaturation temperature. This provides direct proof of i) the presence of a nanometer thick, glycerol-free hydration layer, ii) the high locality of the kinetically limiting process governing renaturation. Graphical abstract: [ABSTRACT FROM AUTHOR]

Objectives:Recent literature suggests that ectopic fat deposition in the pancreas may contribute to endocrine and exocrine organ dysfunction, such as type 2 diabetes (T2D), pancreatitis or pancreatic cancer. The aim of this study was to determine factors associated with pancreatic triglyceride content (PTGC), and to investigate the impact of bariatric surgery on ectopic fat pads, pancreatic fat (PTGC) and hepatic fat (HTGC).Subjects:In all, 45 subjects (13 lean, 13 obese nondiabetics and 19 T2D, matched for age and gender) underwent 1H-magnetic resonance spectroscopy, computed tomography of the visceral abdominal fat, metabolic and lipidomic analysis, including insulin-resistance homeostasis model assessment (HOMA-IR), insulin-secretion homeostasis model assessment (HOMA-B) and plasma fatty-acid composition. Twenty obese subjects were reassessed 6 months after the bariatric surgery.Results:PTGC was significantly higher in type 2 diabetic subjects (23.8±3.2%) compared with obese (14.0±3.3; P=0.03) and lean subjects (7.5±0.9%; P=0.0002). PTGC remained significantly associated with T2D after adjusting for age and sex (β=0.47; P=0.004) or even after adjusting for waist circumference, triglycerides and HOMA-IR (β=0.32; P=0.04). T2D, C18:1n-9 (oleic acid), uric acid, triglycerides and plasminogen activator inhibitor-1 were the five more important parameters involved in PTGC prediction (explained 80% of PTGC variance). Bariatric surgery induced a huge reduction of both HTGC (−51.2±7.9%) and PTGC (−43.8±7.0%) reaching lean levels, whereas body mass index remained greatly elevated. An improvement of insulin resistance HOMA-IR and no change in HOMA-B were observed after bariatric surgery. The PTGC or HTGC losses were not correlated, suggesting tissue-specific mobilization of these ectopic fat stores.Conclusion:Pancreatic fat increased with T2D and drastically decreased after the bariatric surgery. This suggests that decreased PTGC may contribute to improved beta cell function seen after the bariatric surgery. Further, long-term interventional studies are warranted to examine this hypothesis and to determine the degree to which ectopic fat mobilization may mediate the improvement in endocrine and exocrine pancreatic functions. [ABSTRACT FROM AUTHOR]