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[Display omitted] • Western Diet induces metabolic alterations in adult rats. • L. reuteri counteracts the development of Western Diet-induced obesity. • L. reuteri protects the liver from inflammation and oxidative stress. • L. reuteri has a beneficial effect on the liver mitochondrial respiration. • L. reuteri could represent a preventive strategy against diet-related diseases. To evaluate the possible application of Limosilactobacillus reuteri DSM 17938 as a strategy to prevent Western Diet-induced metabolic alterations and liver dysfunction. Male Wistar rats of 90 days were divided in three groups and fed a control diet (CD), a high fat - high fructose diet alone (WD) or in combination with the administration of 108 CFU of L. reuteri (WD-R) for 8 weeks. Body composition, energy balance and plasma lipid profile were evaluated, together with hepatic glucose homeostasis and insulin sensitivity. Metabolic inflammation was also assessed at a whole-body level and in the liver, together with mitochondrial function and oxidative stress. Rats that received the WD and L. reuteri administration exhibited a lower body lipid gain and a higher protein gain, underlying a beneficial effect of the probiotic in counteracting the development of obesity. Moreover, the WD-R rats were protected from the development of inflammation at a whole body and liver level and displayed normal glucose homeostasis and insulin sensitivity, a decreased hepatic lipid deposition and a preserved function of the mitochondrial respiratory chain and redox balance. We demonstrate for the first time that Limosilactobacillus reuteri DSM 17938 has a strong efficacy in preventing the development of the hepatic metabolic derangement elicited by the Western diet administration. These are promising results that open the way for the use of this probiotic as a prevention strategy against the development of diet-related diseases, such as type two diabetes and metabolic syndrome. [ABSTRACT FROM AUTHOR]

Objectives: We assessed the alterations in mitochondrial function in skeletal muscle that were elicited by short-term high-fat feeding in sedentary rats. Methods: Two groups of rats were pair-fed for 1 wk and received a low-fat or high-fat diet. Body composition, energy balance, and glucose homeostasis were measured. Mitochondrial mass, oxidative capacity, and energetic efficiency as well as parameters of oxidative stress and antioxi- dant defense were evaluated in subsarcolemmal and intermyofibrillar mitochondria from the skeletal muscle. Results: Body energy, lipid content, and metabolic efficiency were significantly higher and energy expenditure was significantly decreased among rats that were fed a high-fat diet, as compared with controls. Skeletal muscle mitochondrial energetic efficiency, oxidative capacity for lipid substrates, and antioxidant defense were significantly increased in rats that were fed a high-fat diet as compared with controls. Conclusions: Acute isocaloric high-fat feeding is able to induce increased phosphorylation efficiency in skeletal muscle subsarcolemmal and intermyofibrillar mitochondria. This modification implies a reduced oxidation of energy substrates that may contribute to the early onset of obesity. [ABSTRACT FROM AUTHOR]

Abstract: The objective of the study was to investigate whether changes in liver mitochondrial energetics could underlie the enhanced energetic efficiency that drives accelerated body fat recovery (catch-up fat) during refeeding after caloric restriction. Rats were subjected to caloric restriction (50% of ad libitum intake) for 15 days and then refed for 1 or 2 weeks on an amount of chow equal to that of controls matched for weight at the onset of refeeding. Whole-body metabolism was characterized by energy balance and body composition determinations as well as by indirect calorimetric measurements of 24-hour energy expenditure, substrate oxidation, and whole-body de novo lipogenesis estimated from nonprotein respiratory quotient. Hepatic mitochondrial energetics were determined from measurements of liver mitochondrial mass, respiratory capacities, and proton leak (both basal and fatty acid stimulated), whereas hepatic oxidative status was assessed from measurements of hepatic mitochondrial lipid peroxidation, aconitase, and superoxide dismutase activity. Furthermore, hepatic lipogenic capacity was determined from assays of fatty acid synthase activity. Compared with controls, isocalorically refed rats showed an elevated energetic efficiency and body fat gain over both week 1 and week 2 of refeeding, as well as a lower 24-hour energy expenditure and higher rates of whole-body de novo lipogenesis at the end of both week 1 and week 2 of refeeding. Analysis of the liver revealed that after 1 week (but not after 2 weeks) of refeeding, the mitochondrial mass (but not mitochondrial density) was lower in refed rats than in controls, associated with higher state 3 mitochondrial respiratory capacity, increased superoxide dismutase activity, as well as higher fatty acid synthase activity. These results suggest that, although at the whole-body level elevations in energy efficiency and de novo lipogenesis are coordinated toward catch-up fat, the overall hepatic mitochondrial energetic status during refeeding is more consistent with a contributory role of the liver in the enhanced de novo lipogenic machinery during catch-up fat rather than in the energy-conservation mechanisms (elevated energetic efficiency) that spare energy for catch-up fat. [Copyright &y& Elsevier]

Variations in energy balance, body composition, and nutrient partitioning induced by acetyl-L-carnitine (ALCAR) supplementation were studied in young (2 mo) and old (24 mo) Wistar rats. Changes in skeletal muscle metabolism as well as in serum free triiodothyronine and leptin levels were also evaluated. Rats were administered 0 (control) or 15 g/L ALCAR in their drinking water for 1 mo. ALCAR treatment significantly decreased body lipid percentage in young rats and significantly increased body protein percentage in old rats. The percentage of metabolizable energy (ME) intake stored as lipid was lower in ALCAR-treated young rats, whereas the percentage of ME intake stored as protein was greater in ALCAR-treated old rats compared with their age-matched controls. In addition, ALCAR supplementation significantly decreased serum leptin levels in old rats. Elevated skeletal muscle respiration was found in old rats treated with ALCAR, due to an increase in mitochondrial protein mass. In conclusion, ALCAR supplementation decreases efficiency of lipid deposition in young rats and increases efficiency of protein deposition in old rats. In addition, ALCAR supplementation partly reduces the leptin resistance that occurs in old rats, and improves ATP production in skeletal muscle mitochondria through an increase in mitochondrial protein content. [ABSTRACT FROM AUTHOR]

To investigate whether short term fructose-rich diet induces changes in the gut microbiota as well as in skeletal muscle and adipose tissue physiology and verify whether they persist even after fructose withdrawal, young rats of 30 d of age were fed for 3 weeks a fructose-rich or control diet. At the end of the 3-weeks period, half of the rats from each group were maintained for further 3 weeks on a control diet. Metagenomic analysis of gut microbiota and short chain fatty acids levels (faeces and plasma) were investigated. Insulin response was evaluated at the whole-body level and both in skeletal muscle and epididymal adipose tissue, together with skeletal muscle mitochondrial function, oxidative stress, and lipid composition. In parallel, morphology and physiological status of epididymal adipose tissue was also evaluated. Reshaping of gut microbiota and increased content of short chain fatty acids was elicited by the fructose diet and abolished by switching back to control diet. On the other hand, most metabolic changes elicited by fructose-rich diet in skeletal muscle and epididymal adipose tissue persisted after switching to control diet. Increased dietary fructose intake even on a short-time basis elicits persistent changes in the physiology of metabolically relevant tissues, such as adipose tissue and skeletal muscle, through mechanisms that go well beyond the reshaping of gut microbiota. This picture delineates a harmful situation, in particular for the young populations, posed at risk of metabolic modifications that may persist in their adulthood. [Display omitted] [ABSTRACT FROM AUTHOR]