This study compared the effects of supplementation with a polyphenol-rich pomace from strawberry (US) and a strawberry pomace without most of these c

The present 4-week study on growing Wistar rats was aimed at assessing the potential advantages of dietary supplementation with apple pomace containing both fibre and polyphenols, which enables nutritional exploitation of the physiological traits of both compounds. A total of twenty-four rats, assigned to the control (C), group fed with a diet supplemented with 14 % of processed apple pomace (A) and group fed with a diet supplemented with 15 % unprocessed apple pomace (AP) groups, were fed the following iso-fibrous diets: control, ethanol-extracted and unprocessed apple pomaces (low and high level of dietary polyphenols, i.e. 0·002 and 0·018 %, respectively). To measure the animal response, parameters describing the caecal fermentation, antioxidative status and lipoprotein profile of rats were assessed. Both dietary apple pomaces were found to significantly (P ≤ 0·05) decrease caecal pH and ammonia concentration, microbial β-glucuronidase activity as well as to increase caecal SCFA concentration in comparison to the control diet. The unprocessed pomace did not suppress caecal fermentation. Unlike the extracted one, the dietary apple pomace rich in polyphenols significantly (P ≤ 0·05v. C group) increased erythrocyte superoxide dismutase activity and serum antioxidant capacity of lipid-soluble substances and significantly (P ≤ 0·05v. C group) decreased amounts of thiobarbituric acid-reactive substances in liver tissue. Moreover, the 4-week administration of the AP diet to rats evoked a significant decrease in serum glucose concentration (P ≤ 0·05v. C and A groups). In conclusion, the results demonstrated that the polyphenol-rich fibre complexes from apple pomace exerted positive effects on gastrointestinal physiology and antioxidant status of rats.

The mechanism by which mice, exposed to the cold, mobilize endogenous or exogenous fuel sources for heat production is unknown. To address this issue we carried out experiments using 3 models of obesity in mice: C57BL/6J+/+ (wild-type B6) mice with variable susceptibility to obesity in response to being fed a high-fat diet (HFD), B6. Ucp1-/- mice with variable diet-induced obesity (DIO) and a deficiency in brown fat thermogenesis and B6. Lep-/- with defects in thermogenesis, fat mobilization and hyperphagia. Mice were exposed to the cold and monitored for changes in food intake and body composition to determine their energy balance phenotype. Upon cold exposure wild-type B6 and Ucp1-/- mice with diet-induced obesity burned endogenous fat in direct proportion to their fat reserves and changes in food intake were inversely related to fat mass, whereas leptin-deficient and lean wild-type B6 mice fed a chow diet depended on increased food intake to fuel thermogenesis. Analysis of gene expression in the hypothalamus to uncover a central regulatory mechanism revealed suppression of the Npvf gene in a manner that depends on the reduced ambient temperature and degree of exposure to the cold, but not on adiposity, leptin levels, food intake or functional brown fat. Current knowledge does not provide a clear, definite view of central mechanisms controlling energy balance upon cold-activated thermogenesis. Here we show that upon cold exposure lean mice maintain body composition but increase food intake to fuel thermogenesis, whereas cold-exposed mice with DIO utilize endogenous fat stores and then transition to increased food intake as body composition approaches that of the lean controls. Using knockout mice with leptin and Ucp1 gene deficiency our study indicates that the relative energy utilization from food intake and endogenous energy reserves to maintain body temperature during cold exposure is independent of both leptin action and brown fat-linked thermogenesis. Using a combination of genetic and biological approaches, we demonstrate that Npvf gene expression in the hypothalamus is regulated by changes in ambient temperature in a manner independent of the nutritional status of the mouse.

The effects of feeding soluble dietary fibre (inulin, I) separately or in combination with insoluble fibre (cellulose, CEL) on caecal fermentation and biochemical blood parameters were studied in rats. Four diets: CEL-rich (10%) and CEL-free, each supplemented with 5% of sucrose or I (CR, CF, CRI...

The objective of the study was to compare the effects of experimentally induced type 1 or type 2 diabetes (T1D or T2D) on the functional, structural and biochemical properties of mouse peripheral nerves. Eight-week-old C57BL/6 mice were randomly assigned into three groups, including the control (CTRL, chow-fed), STZ (streptozotocin (STZ)-injected), and HFD (high-fat diet (HFD)-fed) group. After 18-weeks of experimental treatment, HFD mice had higher body weights and elevated levels of plasma lipids, while STZ mice developed hyperglycemia. STZ-treated mice, after an extended period of untreated diabetes, developed motor and sensory nerve conduction-velocity deficits. Moreover, relative to control fibers, pre- and diabetic axons were lower in number and irregular in shape. Animals from both treatment groups manifested a pronounced overexpression of nNOS and a reduced expression of SOD1 proteins in the sciatic nerve, indicating oxidative–nitrosative stress and ineffective antioxidant protection in the peripheral nervous system of these mice. Collectively, STZ- and HFD-treated mice revealed similar characteristics of peripheral nerve damage, including a number of morphological and electrophysiological pathologies in the sciatic nerve. While hyperglycemia is a large component of diabetic neuropathy pathogenesis, the non-hyperglycemic effects of diabetes, including dyslipidemia, may also be of importance in the development of this condition.