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210 results on '"Crescenzo, Raffaella"'

4. Limosilactobacillus reuteri DSM 17938 reverses gut metabolic dysfunction induced by Western diet in adult rats

Author

Abuqwider, Jumana, primary, Di Porzio, Angela, additional, Barrella, Valentina, additional, Gatto, Cristina, additional, Sequino, Giuseppina, additional, De Filippis, Francesca, additional, Crescenzo, Raffaella, additional, Spagnuolo, Maria Stefania, additional, Cigliano, Luisa, additional, Mauriello, Gianluigi, additional, Iossa, Susanna, additional, and Mazzoli, Arianna, additional

Published
2023
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6. Cabergoline counteracts adipose and skeletal muscle lipid accumulation through promoting oxidative pathway: an in vivo and in vitro preclinical study

Author

Negri, Mariarosaria, primary, Pivonello, Claudia, additional, Amatrudo, Feliciana, additional, Patalano, Roberta, additional, Monto, Tatiana, additional, Paola, Provvisiero Donatella, additional, Simeoli, Chiara, additional, de, Angelis Cristina, additional, Simona, Auriemma Renata, additional, Colao, Annamaria, additional, Crescenzo, Raffaella, additional, and Pivonello, Rosario, additional

Published
2023
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18. Acetyl-L-carnitine supplementation differently influences nutrient partitioning, serum leptin concentration and skeletal muscle mitochondrial respiration in young and old rats

Author

Iossa, Susanna, Mollica, Maria Pina, Lionetti, Lilla, Crescenzo, Raffaella, Botta, Monica, Barletta, Antonio, and Liverini, Giovanna

Subjects
Striated muscle -- Physiological aspects, Acetyl-L-carnitine -- Physiological aspects, Body composition -- Measurement, Leptin -- Physiological aspects, Food/cooking/nutrition
Abstract

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. J. Nutr. 132: 636-642, 2002. KEY WORDS: * acetyl-L-carnitine * aging * energy balance * skeletal muscle * leptin * rats

Published
2002

20. A Short‐Term Western Diet Impairs Cholesterol Homeostasis and Key Players of Beta Amyloid Metabolism in Brain of Middle Aged Rats

Author

Spagnuolo, Maria Stefania, primary, Pallottini, Valentina, additional, Mazzoli, Arianna, additional, Iannotta, Lucia, additional, Tonini, Claudia, additional, Morone, Barbara, additional, Ståhlman, Marcus, additional, Crescenzo, Raffaella, additional, Strazzullo, Maria, additional, Iossa, Susanna, additional, and Cigliano, Luisa, additional

Published
2020
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32. Brain Nrf2 pathway, autophagy, and synaptic function proteins are modulated by a short-term fructose feeding in young and adult rats.

Author

Spagnuolo, Maria Stefania, Bergamo, Paolo, Crescenzo, Raffaella, Iannotta, Lucia, Treppiccione, Lucia, Iossa, Susanna, and Cigliano, Luisa

Subjects
FRUCTOSE, YOUNG adults, GLUTATHIONE reductase, RATS, BRAIN-derived neurotrophic factor, NUTRITIONAL requirements
Abstract

Objectives: A strong rise of the fructose content in the human diet occurred in the last decade, as corn syrup is widely used as a sweetener for beverages and processed food. Since young people make a widespread consumption of added sugars, we evaluated the effects of a two weeks fructose-rich diet on brain redox homeostasis, autophagy and synaptic plasticity in the cortex of young and adults rats, in order to highlight the early risks to which brain is exposed. Methods and Results: Short-term fructose feeding was associated with an imbalance of redox homeostasis, as lower amount of Nuclear factor (erythroid derived 2)-like 2, lower activity of Glucose 6-phosphate dehydrogenase and Glutathione reductase, together with lower Glutathione/Oxidized Glutathione ratio, were found in fructose-fed young and adult rats. Fructose-rich diet was also associated with the activation of autophagy, as higher levels of Beclin, LC3 II and P62 were detected in cortex of fructose-fed rats. A diet associated decrease of synaptophysin, synapsin I, and synaptotagmin I, was found in fructose-fed young and adult rats. Interestingly, BDNF amount was significantly lower only in fructose-fed adult rats, while the level of its receptor TrkB decreased in both groups of treated rats. A further marker of brain functioning, Acetylcholinesterase activity, was found increased only in fructose-fed young animals. Conclusion: Overall, our findings suggest that young rats may severely suffer from the deleterious influence of fructose on brain health as the adults and provide experimental data suggesting the need of targeted nutritional strategies to reduce its amount in foods. [ABSTRACT FROM AUTHOR]

Published
2020
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39. Mitochondrial energetics in liver and skeletal muscle after energy restriction in young rats

Author

Crescenzo, Raffaella, Bianco, Francesca, Falcone, Italia, Coppola, Paola, Dulloo, Abdul G., Liverini, Giovanna, Iossa, Susanna, Crescenzo, Raffaella, Bianco, Francesca, Falcone, Italia, Coppola, Paola, Dulloo, Abdul G., Liverini, Giovanna, and Iossa, Susanna

Abstract

The present study investigated the effect of 2 weeks of energy restriction on whole body, liver and skeletal muscle energy handling. We measured whole-body oxygen consumption, as well as mitochondrial protein mass, respiratory capacity and energetic coupling in liver and skeletal muscle from food-restricted (FR) rats, age- and weight-matched controls. We also assessed markers of oxidative damage and antioxidant defences. The present results show that, in response to energy restriction, an adaptive decrease in whole-body energy expenditure is coupled with structural and functional changes in mitochondrial compartment, both in liver and skeletal muscle. In fact, liver mitochondrial mass per g of liver significantly increased, whereas total hepatic mitochondrial oxidative capacity was lower in FR than in control rats, because of a significant decrease in liver contribution to total body weight. In skeletal muscle, sub-sarcolemmal (SS) mitochondrial respiratory capacity, as well as SS and inter-myofibrillar (IMF) mitochondrial protein mass per g of tissue, was significantly lower in FR rats, compared to controls. Finally, a decrease in oxidative damage was found in liver but not in skeletal muscle mitochondria from FR rats, whereas an increase in antioxidant defence was found in both tissues. From the present results, it appears that skeletal muscle is involved in the decrease in energy expenditure induced by energy restriction. Energy sparing is achieved through changes in the activity (SS), mass (SS and IMF) and efficiency (IMF) of mitochondrial compartment

Published
2017

40. Polyunsaturated fatty acids stimulate de novo lipogenesis and improve glucose homeostasis during refeeding with high fat diet

Author

Crescenzo, Raffaella, Mazzoli, Arianna, Cancelliere, Rosa, Bianco, Francesca, Giacco, Antonia, Liverini, Giovanna, Dulloo, Abdul G., Iossa, Susanna, Crescenzo, Raffaella, Mazzoli, Arianna, Cancelliere, Rosa, Bianco, Francesca, Giacco, Antonia, Liverini, Giovanna, Dulloo, Abdul G., and Iossa, Susanna

Abstract

The recovery of body weight after a period of caloric restriction is accompanied by an enhanced efficiency of fat deposition and hyperinsulinemia—which are exacerbated by isocaloric refeeding on a high fat diet rich in saturated and monounsaturated fatty acids (SFA-MUFA), and poor in polyunsaturated fatty acids (PUFA), and associated with a blunting of de novo lipogenesis in adipose tissue and liver. As high fat diets rich in PUFA have been shown to limit the excess fat deposition and improve glucose homeostasis, we investigated here the extent to which de novo lipogenesis in liver and adipose tissues (white and brown), as well as hepatic oxidative stress, are influenced by refeeding on diets rich in PUFA.Design: In rats calorically restricted for 14 days and refed for 14 days on isocaloric amounts of a high fat diet rich in lard (i.e., high SFA- MUFA) or in safflower and linseed oils (rich in PUFA), we investigated energy balance, body composition, glycemic profile, and the regulation of fatty acid synthase (rate- limiting enzyme of de novo lipogenesis) in liver, white and brown adipose tissue. We also evaluated oxidative stress in liver and skeletal muscle and markers of hepatic inflammation.Results: Rats refed the PUFA diet gained less lipids and more proteins compared to rats refed SFA-MUFA diet and showed lower amount of visceral and epididymal white adipose tissue, but increased depots of interscapular brown adipose tissue, with higher expression of the uncoupling protein 1. A significant increase in non- protein respiratory quotient and carbohydrate utilization was found in rats refed PUFA diet. Rats refed PUFA diet showed improved glucose homeostasis, as well as lower triglycerides and cholesterol levels. Fatty acid synthase activity was significantly higher in liver, white and brown adipose tissue, while lipid peroxidation and the degree of inflammation in the liver were significantly lower, in rats refed PUFA diet.Conclusions: When considering the composit

Published
2017

43. PACAP and PACAP receptors in adipose tissue of rats fed with high fructose diet

Author

VALIANTE, Salvatore, CRESCENZO, RAFFAELLA, CAPALDO, ANNA, IOSSA, SUSANNA, LAFORGIA, VINCENZA, DE FALCO, MARIA, Sellitti A, Salamone S, Italian society of Histochemistry, University of Pavia, Valiante, Salvatore, Crescenzo, Raffaella, Sellitti, A, Capaldo, Anna, Salamone, S, Iossa, Susanna, Laforgia, Vincenza, and DE FALCO, Maria

Published
2011

47. OMEGA-6-FATTY ACIDS RICH DIETS DECREASE LIVER MITOCHONDRIAL EFFICIENCY DURING REFEEDING AFTER CALORIC RESTRICTION IN RAT

Author

CRESCENZO, RAFFAELLA, FALCONE, ITALIA, LIVERINI, GIOVANNA, IOSSA, SUSANNA, BIANCO F., YEPURI G., DULLOO A.G., Crescenzo, Raffaella, Bianco, F., Falcone, Italia, Yepuri, G., Dulloo, A. G., Liverini, Giovanna, and Iossa, Susanna

Abstract

Catch-up growth - a risk for later obesity and type 2 diabetes - is characterized by a higher rate of fat relative to lean tissue deposition. Using a rat model of refeeding after semistarvation, such catch-up fat has been shown to be primarily driven by suppressed thermogenesis and to be exacerbated by high-fat diets rich in animal (saturated) fats. This latter exacerbation of catch-up fat is however not observed with safflower oil - which is rich in omega-6 polyunsaturated fatty acids; these anti-obesity effects being explained partly by a higher lean tissue deposition and partly by enhanced thermogenesis. We investigated here the role of altered liver mitochondrial energy coupling and relative oxidative stress (assessed as SOD specific activity) in such dietary modulation of catch-up fat. After 14 days of semistarvation, male Sprague-Dawley rats were refed for 7 days with isocaloric amounts of either a low-fat diet, a high-fat lard diet or high-fat safflower oil diet. Compared to the group refed the high-fat lard diet, the rats refed isocalorically on high-fat safflower oil diet gained less body fat but more body protein, and their isolated liver mitochondria showed increased proton leak (basal and palmitate-induced) and decreased oxidative stress. Thus the exaggerated suppression of thermogenesis that exacerbates catch-up fat on high-fat diets is counteracted by a diet rich in omega-6 fatty acids, in part by a shift in energy partitioning from body fat to protein, and in part via increased thermogenesis resulting from increased hepatic mitochondrial proton leak and decreased mitochodrial efficiency.

Published
2008

48. Alterations in hepatic mitochondrial compartment in a model of obesity and insulin resistance

Author

Prisco Marina, Iossa Susanna, Crescenzo Raffaella, Falcone Italia, Liverini Giovanna, Bianco Francesca, Crescenzo, Raffaella, Bianco, Francesca, Falcone, Italia, Prisco, Marina, Liverini, Giovanna, and Iossa, Susanna

Subjects
Blood Glucose, Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Cell Respiration, Medicine (miscellaneous), Mitochondria, Liver, Mitochondrion, medicine.disease_cause, Lipid peroxidation, Superoxide dismutase, chemistry.chemical_compound, Endocrinology, Insulin resistance, Internal medicine, medicine, Citrate synthase, Glucose homeostasis, Animals, Insulin, Obesity, Rats, Wistar, Aconitate Hydratase, Nutrition and Dietetics, biology, Superoxide Dismutase, Carbon Dioxide, medicine.disease, Dietary Fats, Rats, Respiratory quotient, Fatty Liver, Disease Models, Animal, chemistry, biology.protein, Lipid Peroxidation, Insulin Resistance, Oxidative stress
Abstract

The objective of this paper is to evaluate adaptations in hepatic mitochondrial protein mass, function and efficiency in a rat model of high-fat diet-induced obesity and insulin resistance that displays several correlates to human obesity. Adult male rats were fed a high-fat diet for 7 weeks. Mitochondrial state 3 and state 4 respiratory capacities were measured in liver homogenate and isolated mitochondria by using nicotinamide adenine dinucleotide, flavin adenine dinucleotide and lipid substrates. Mitochondrial efficiency was evaluated by measuring proton leak kinetics. Mitochondrial mass was assessed by ultrastructural observations and citrate synthase (CS) activity measurements. Mitochondrial oxidative damage and antioxidant defence were also considered by measuring lipid peroxidation, aconitase and superoxide dismutase (SOD) specific activity. Whole body metabolic characteristics were obtained by measuring 24-h oxygen consumption (VO2), carbon dioxide production (VCO2), respiratory quotient (RQ) and nonprotein respiratory quotient (NPRQ), using indirect calorimetry with urinary nitrogen analysis. Whole body glucose homeostasis was assessed by measuring plasma insulin and glucose levels after a glucose load. Adult rats fed a high-fat diet for 7 weeks, exhibit not only obesity, insulin resistance and hepatic steatosis, but also reduced respiratory capacity and increased oxidative stress in liver mitochondria. Our present results indicate that alterations in the mitochondrial compartment induced by a high-fat diet are associated with the development of insulin resistance and ectopic fat storage in the liver. Our results thus fit in with the emerging idea that mitochondrial dysfunction can led to the development of metabolic diseases, such as obesity, type 2 diabetes mellitus and nonalcoholic steatohepatitis.

Published
2008

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