Effect of high-fat feeding on metabolic efficiency and mitochondrial oxidative capacity in adult rats

Iossa, Susanna; Lionetti, Lillà; Mollica, Maria Pina; Crescenzo, Raffaella; Botta, Monica; Barletta, Antonio; Liverini, Giovanna

doi:10.1079/bjn2003000968

Cited by 113 publications

(79 citation statements)

References 44 publications

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“…In fact, in a previous work, we showed that 90 days old Wistar rats fed this high-fat diet for 2 weeks exhibited an increase in fat storage without any change in NEFA, glucose and insulin Subsarcolemmal mitochondria and high-fat diet L Lionetti et al levels. 18 It can be suggested that the length of high-fat treatment is an important factor in the development of glucose homeostasis impairment in adult Wistar rats. Our present results also show a decreased oxidative capacity in SS mitochondria isolated from rats fed high-fat diet, in agreement with a recent study demonstrating a downregulation in genes involved in oxidative phosphorylation both in man and mice fed on diets rich in fat.…”

Section: Discussionmentioning

confidence: 99%

“…17 We have previously shown that 90-day-old Wistar rats fed a high-fat diet for 2 weeks became obese, but did not develop insulin resistance, since they exhibited serum insulin and glucose levels similar to those found in control rats fed a lowfat diet. 18 The current study was therefore designed to determine the impact of a longer term high-fat feeding on energy balance and glucose homeostasis. Another purpose of this study was to evaluate skeletal muscle mitochondrial functionality, by determining mitochondrial oxidative activity and energetic efficiency in rats in which obesity was induced by a long-term high-fat feeding.…”

Section: Introductionmentioning

confidence: 99%

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Skeletal muscle subsarcolemmal mitochondrial dysfunction in high-fat fed rats exhibiting impaired glucose homeostasis

et al. 2007

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Objective: To investigate whether changes in body energy balance induced by long-term high-fat feeding in adult rats could be associated with modifications in energetic behaviour and oxidative stress of skeletal muscle subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondrial populations. Design: Adult rats were fed low-fat or high-fat diet for 7 weeks. Measurements: Body energy balance and composition analysis together with plasma insulin and glucose level determination in the whole animal. Oxidative capacity, basal and induced proton leaks as well as aconitase and superoxide dismutase activities in SS and IMF mitochondria from skeletal muscle. Results: High-fat fed rats exhibit increased body lipid content, as well as hyperinsulinemia, hyperglycaemia and higher plasma non-esterified fatty acids. In addition, SS mitochondria display lower respiratory capacity and a different behaviour of SS and IMF mitochondria is found in the prevention from oxidative damage. Conclusions: A deleterious consequence of decreased oxidative capacity in SS mitochondria from rats fed high-fat diet would be a reduced utilization of energy substrates, especially fatty acids, which may lead to intracellular triglyceride accumulation, lipotoxicity and insulin resistance development. Our results thus reveal a possible role for SS mitochondria in the impairment of glucose homeostasis induced by high-fat diet.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Skeletal muscle subsarcolemmal mitochondrial dysfunction in high-fat fed rats exhibiting impaired glucose homeostasis

et al. 2007

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“…Mitochondrial respiration, proton leak, lipid peroxidation, aconitase, and SOD specific activity Liver homogenates and isolated mitochondria were prepared as previously reported [13]. Control experiments of enzymatic and electron microscopy characterization have shown that our isolation procedure (centrifugation at 3000g av http://doc.rero.ch for 10 minutes) results in a cellular fraction essentially constituted by mitochondria.…”

Section: Mitochondrial Ultrastructural Observations and Mitochondrialmentioning

confidence: 99%

Hepatic mitochondrial energetics during catch-up fat after caloric restriction

et al. 2010

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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.

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“…In a dietetic context, nutritional intervention by means of a hypocaloric diet reduced the habitual fat intake of volunteers. These dietary changes could produce protective effects against redox imbalance, since a high fat intake decreases the mitochondrial oxidation capacity as demonstrated in animal models (Iossa et al, 2003).…”

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confidence: 99%

Postprandial insulin response and mitochondrial oxidation in obese men nutritionally treated to lose weight

2004

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Obesity, hyperglycemia, and insulin resistance have been associated to an oxidative mitochondrial dysfunction. The aim of this research was to evaluate the relation between carbohydrate metabolism and mitochondrial oxidation, as affected by the weight status and the weight loss induced by a calorie-restricted diet. Lean control men (BMIo25 kg/m 2 , n ¼ 6) and obese men (BMI430 kg/m 2 , n ¼ 14), who were characterized as insulin resistant (n ¼ 6) or insulin sensitive (n ¼ 8) based on HOMA index values, participated in the trial. Plasma insulin levels and mitochondrial oxidation estimated by the 2-keto(1-13 C)isocaproate breath test, were measured after ingestion of a test meal during 3 h. Obese subjects repeated the breath test protocol after a 10-week caloric restriction diet to lose weight. Postprandial insulin secretion tended to be marginally higher (P ¼ 0.059) in both obese groups than in controls, while the rate of postprandial mitochondrial oxidation was markedly decreased (P ¼ 0.019) in the obese subjects as compared with lean individuals. The nutritionally induced weight loss produced a rise in the postprandial oxidative process in volunteers initially considered as insulin resistant (P ¼ 0.036), while no statistical differences in the insulin-sensitive obese (P ¼ 0.241) were found. Interestingly, the percentage of oxidized tracer was inversely related to postprandial insulin secretion (r ¼ À0.56; P ¼ 0.001). In conclusion, these results support the hypothetized relation between carbohydrate metabolism and mitochondrial oxidation at a postprandial state in obese subjects, raising interest about mitochondria stimulation as a target in the therapy of obesity.

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Effect of high-fat feeding on metabolic efficiency and mitochondrial oxidative capacity in adult rats

Cited by 113 publications

References 44 publications

Skeletal muscle subsarcolemmal mitochondrial dysfunction in high-fat fed rats exhibiting impaired glucose homeostasis

Skeletal muscle subsarcolemmal mitochondrial dysfunction in high-fat fed rats exhibiting impaired glucose homeostasis

Hepatic mitochondrial energetics during catch-up fat after caloric restriction

Postprandial insulin response and mitochondrial oxidation in obese men nutritionally treated to lose weight

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