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We study the stress response to a step strain of covalently bonded gelatin gels in the temperature range where triple helix reversible crosslink formation is prohibited. We observe slow stress relaxation towards a T-dependent finite asymptotic level. We show that this is assignable to the strain-induced coil → helix transition, previously evidenced by Courty et al. [Proc. Natl. Acad. Sci. U. S. A. 102, 13457 (2005)], of a fraction of the polymer strands. Relaxation proceeds, in a first stage, according to a stretched exponential dynamics, then crosses over to a terminal simple exponential decay. The respective characteristic times TK and Tf exhibit an Arrhenius-like T-dependence with an associated energy E incompatibly larger than the activation barrier height for the isomerisation process which sets the clock for an elementary coil → helix transformation event. We tentatively assign this glass-like slowing down of the dynamics to the long-range couplings due to the mechanical noise generated by the local elementary events in this random elastic medium. [ABSTRACT FROM AUTHOR]

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]

We probe the mechanisms at work in the build-up of thermoreversible gel networks, with the help of hybrid gelatin gels containing a controlled density of irreversible, covalent crosslinks (CLs), which we quench below the physical gelation temperature. The detailed analysis of the dependence on covalent crosslink density of both the shear modulus and optical activity evolutions with time after quench enables us to identify two stages of the physical gelation process, separated by a temperature-dependent crossover modulus: (i) an early nucleation regime during which rearrangements of the triple-helix CLs play a negligible role, and (ii) a late, logarithmic aging one, which is preserved, though slowed down, in the presence of irreversible CLs. We show that aging is fully controlled by rearrangements and discuss the implication of our results in terms of the switch from an early, local dynamics to a late, cooperative long-range one. [ABSTRACT FROM AUTHOR]

We study the interplay between a crack tip slowly propagating through a hydrogel and nanoparticles suspended in its liquid environment. Using a proteinic gel enables us to tune the electrostatic interaction between the network and silica colloids. Thereby, we unveil two distinct, local toughening mechanisms. The primary one is charge independent and involves the convective building of a thin particulate clog, hindering polymer hydration in the crack process zone. When particles and network bear opposite charges, transient adhesive bonding superimposes, permitting the remarkable pinning of a crack by a liquid drop. [ABSTRACT FROM AUTHOR]

Aim To conduct a prospective randomized trial to investigate the effect of glucagon-like peptide-1 ( GLP-1) analogues on ectopic fat stores. Methods A total of 44 obese subjects with type 2 diabetes uncontrolled on oral antidiabetic drugs were randomly assigned to receive exenatide or reference treatment according to French guidelines. Epicardial adipose tissue ( EAT), myocardial triglyceride content ( MTGC), hepatic triglyceride content ( HTGC) and pancreatic triglyceride content ( PTGC) were assessed 45 min after a standardized meal with 3T magnetic resonance imaging and proton magnetic resonance spectroscopy before and after 26 weeks of treatment. Results The study population had a mean glycated haemoglobin ( HbA1c) level of 7.5 ± 0.2% and a mean body mass index of 36.1 ± 1.1 kg/m2. Ninety five percent had hepatic steatosis at baseline ( HTGC ≥ 5.6%). Exenatide and reference treatment led to a similar improvement in HbA1c (−0.7 ± 0.3% vs. −0.7 ± 0.4%; p = 0.29), whereas significant weight loss was observed only in the exenatide group (−5.5 ± 1.2 kg vs. −0.2 ± 0.8 kg; p = 0.001 for the difference between groups). Exenatide induced a significant reduction in EAT (−8.8 ± 2.1%) and HTGC (−23.8 ± 9.5%), compared with the reference treatment ( EAT: −1.2 ± 1.6%, p = 0.003; HTGC: +12.5 ± 9.6%, p = 0.007). No significant difference was observed in other ectopic fat stores, PTGC or MTGC. In the group treated with exenatide, reductions in liver fat and EAT were not associated with homeostatic model assessment of insulin resistance index, adiponectin, HbA1c or fructosamin change, but were significantly related to weight loss (r = 0.47, p = 0.03, and r = 0.50, p = 0.018, respectively). Conclusion Our data indicate that exenatide is an effective treatment to reduce liver fat content and epicardial fat in obese patients with type 2 diabetes, and these effects are mainly weight loss dependent. [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]