Dietary effects on pelage emissivity in mammals: Implications for infrared thermography.

Infrared thermography is becoming popular to measure animal surface temperature non-invasively. However, its application in quantitative mammal research is restricted by a paucity of pelage emissivity measurements, which are necessary to acquire accurate temperature readings. Furthermore, the factors influencing pelage emissivity remain largely unknown. We therefore examined the putative links between diet (fat content), hair length, hair diameter, and pelage emissivity in laboratory mice. Individuals maintained on high-fat diets had higher pelage emissivity values than those on standard diets, which may be due to fur being oily and/or the fact that the fur clumped together, exposing the skin underneath. Alternatively, the chemical composition of the fur of individuals on a high-fat diet may vary from those on a standard diet. We found no significant relationships between various hair metrics and emissivity. This study highlights that aspects of an animal's life history (e.g. age, sex, diet) may contribute to the emissivity of its pelage. As such, a single emissivity value may be inappropriate for use in infrared thermography across all species or individuals; other aspects of an animal's biology, which may affect emissivity, should also be considered. Best practice should involve measuring emissivity for every individual animal used in thermography studies.

Treatment of lean and diet-induced obesity (DIO) mice with a novel stable obestatin analogue alters plasma metabolite levels as detected by untargeted LC-MS metabolomics.

INTRODUCTION: Obestatin is a controversial gastrointestinal peptide purported to have metabolic actions. OBJECTIVES: This study investigated whether treatment with a stable obestatin analogue (PEG-OB(Cys10, Cys13)) changed plasma metabolite levels firstly in lean and subsequently in diet-induced obesity (DIO) C57BL6/J mice. METHODS: Untargeted LC-HRMS metabolomics experiments were carried out in ESI + mode with plasma extracts from both groups of animals. Data were normalised, multivariate and univariate statistical analysis performed and metabolites of interest putatively identified. RESULTS: In lean mice, 39 metabolites were significantly changed by obestatin treatment and the majority of these were increased, including various C16 and C18 moieties of phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine and monoacylglycerol, along with vitamin A, vitamin D3, tyrosine, acetylcarnitine and 2α-(hydroxymethyl)-5α-androstane-3ß,17ß-diol. Decreased concentrations of glycolithocholic acid, 3-dehydroteasterone and various phospholipids were observed. In DIO mice, 25 metabolites were significantly affected and strikingly, the magnitudes of changes here were generally much greater in DIO mice than in lean mice, and in contrast, the majority of metabolite changes were decreases. Four metabolites affected in both groups included glycolithocholic acid, and three different long-chain (C18) phospholipid molecules (phosphatidylethanolamine, platelet activating factor (PAF), and monoacylglycerol). Metabolites exclusively affected in DIO mice included various phosphatidylcholines, lysophosphatidylcholines and fatty acyls, as well as creatine and oxidised glutathione. CONCLUSION: This investigation demonstrates that obestatin treatment affects phospholipid turnover and influences lipid homeostasis, whilst providing convincing evidence that obestatin may be acting to ameliorate diet-induced impairments in lipid metabolism, and it may influence steroid, bile acid, PAF and glutathione metabolism.

Obestatin as a key regulator of metabolism and cardiovascular function with emerging therapeutic potential for diabetes.

Obestatin is a 23-amino acid C-terminally amidated gastrointestinal peptide derived from preproghrelin and which forms an α helix. Although obestatin has a short biological half-life and is rapidly degraded, it is proposed to exert wide-ranging pathophysiological actions. Whilst the precise nature of many of its effects is unclear, accumulating evidence supports positive actions on both metabolism and cardiovascular function. For example, obestatin has been reported to inhibit food and water intake, body weight gain and gastrointestinal motility and also to mediate promotion of cell survival and prevention of apoptosis. Obestatin-induced increases in beta cell mass, enhanced adipogenesis and improved lipid metabolism have been noted along with up-regulation of genes associated with beta cell regeneration, insulin production and adipogenesis. Furthermore, human circulating obestatin levels generally demonstrate an inverse association with obesity and diabetes, whilst the peptide has been shown to confer protective metabolic effects in experimental diabetes, suggesting that it may hold therapeutic potential in this setting. Obestatin also appears to be involved in blood pressure regulation and to exert beneficial effects on endothelial function, with experimental studies indicating that it may also promote cardioprotective actions against, for example, ischaemia-reperfusion injury. This review will present a critical appraisal of the expanding obestatin research area and discuss the emerging therapeutic potential of this peptide for both metabolic and cardiovascular complications of diabetes.