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3. 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

4. Nonthyrotoxic prevention of diet-induced insulin resistance by 3,5-diiodo-L-thyronine in rats

Author

de Lange, Pieter, Cioffi, Federica, Senese, Rosalba, Moreno, Maria, Lombardi, Assunta, Silvestri, Elena, De Matteis, Rita, Lionetti, Lilla, Mollica, Maria Pina, Goglia, Fernando, and Lanni, Antonia

Subjects
Ketogenic diet -- Health aspects, Diabetes -- Care and treatment -- Prevention -- Research, Insulin resistance -- Care and treatment -- Prevention -- Research, Health
Abstract

OBJECTIVE--High-fat diets (HFDs) are known to induce insulin resistance. Previously, we showed that 3,5-diiodothyronine (T2), concomitantly administered to rats on a 4-week HFD, prevented gain in body weight and adipose mass. Here we investigated whether and how T2 prevented HFD-induced insulin resistance. RESEARCH DESIGN AND METHODS--We investigated the biochemical targets of T2 related to lipid and glucose homeostasis over time using various techniques, including genomic and proteomie profiling, immunoblotting, transient transfection, and enzyme activity analysis. RESULTS--Here we show that, in rats, HFD feeding induced insulin resistance (as expected), whereas T2 administration prevented its onset. T2 did so by rapidly stimulating hepatic fatty acid oxidation, decreasing hepatic triglyceride levels, and improving the serum lipid profile, while at the same time sparing skeletal muscle from fat accumulation. At the mechanistic level, 1) transfection studies show that T2 does not act via thyroid hormone receptor β; 2) AMP-activated protein kinase is not involved in triggering the effects of T2; 3) in HFD rats, T2 rapidly increases hepatic nuclear sirtuin 1 (SIRT1) activity; 4) in an in vitro assay, T2 directly activates SIRT1; and 5) the SIRT1 targets peroxisome proliferator-activated receptor (PPAR)-γ coactivator (PGC-1α) and sterol regulatory element-binding protein (SREBP)-1c are deacetylated with concomitant upregulation of genes involved in mitochondrial biogenesis and downregulation of lipogenic genes, and PPAR[alpha/δ-induced genes are upregulated, whereas genes involved in hepatic gluconeogenesis are downregulated. Proteomic analysis of the hepatic protein profile supported these changes. CONCLUSIONS--T2, by activating SIRT1, triggers a cascade of events resulting in improvement of the serum lipid profile, prevention of fat accumulation, and, finally, prevention of diet-induced insulin resistance. Diabetes 60:2730-2739, 2011, Obesity and associated disorders (including insulin resistance, glucose intolerance, dyslipidemia, and hypertension) are approaching epidemic proportions worldwide (1,2). Increasing lipid oxidation in the liver is a key target for improving [...]

Published
2011
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5. Energy intake and utilization vary during development in rats

Author

Iossa, Susanna, Lionetti, Lilla, Mollica, Maria Pina, Barletta, Antonio, and Liverini, Giovanna

Subjects
Energy metabolism -- Research, Rats -- Food and nutrition, Leptin -- Research, Food/cooking/nutrition
Abstract

Energy intake, utilization, and partitioning were determined in male Wistar rats from 25 to 180 d of age. Serum free triiodothyronine, leptin, and free fatty acid concentrations were also measured. Energy balance measurements allowed us to identify a period from 25 to 90 d, characterized by a rapid body growth rate and another from 90 to 180 d, during which body growth rate slowed. From 25 to 180 d, we found decreases in daily energy intake and expenditure, which were faster before 90 d. The first period was characterized by storage of lipid and protein. In the second period, protein deposition approached zero and the excess of ingested energy was entirely stored as fat, so that age-associated obesity began to develop. The inability of rats to maintain a stable body weight after the cessation of growth of lean body mass is not due to decreased resting metabolism but rather to a partial leptin resistance. KEY WORDS: energy balance measurements; resting metabolic rate; leptin; developing rats

Published
1999

9. Altered skeletal muscle subsarcolemmal mitochondrial compartment during catch-up fat after caloric restriction

Author

Crescenzo, Raffaella, Lionetti, Lilla, Mollica, Maria Pina, Ferraro, Marialuisa, D'Andrea, Elvira, Mainieri, Davide, Dulloo, Abdul G., Liverini, Giovanna, and Iossa, Susanna

Subjects
Cardiovascular diseases -- Risk factors -- Care and treatment, Type 2 diabetes -- Risk factors -- Care and treatment, Health, Care and treatment, Risk factors
Abstract

An accelerated rate of fat recovery (catch-up fat) and insulin resistance are characteristic features of weight recovery after caloric restriction, with implications for the pathophysiology of catch-up growth and weight fluctuations. Using a previously described rat model of weight recovery in which catch-up fat and skeletal muscle insulin resistance have been linked to suppressed thermogenesis per se, we investigated alterations in mitochondrial energetics and oxidative stress in subsarcolemmal (SS) and intermyofibrillar (IMF) skeletal muscle mitochondria. After 2 weeks of semistarvation followed by 1 week of refeeding, the refed rats show persistent and selective reductions in SS mitochondrial mass (assessed from citrate synthase activity in tissue homogenate and isolated mitochondria) and oxidative capacity. Furthermore, the refed rats show, in both SS and IMF muscle mitochondria, a lower aconitase activity (whose inactivation is an index of increased reactive oxygen species [ROS]), associated with higher superoxide dismutase activity and increased proton leak. Taken together, these studies suggest that diminished skeletal muscle mitochondrial mass and function, specifically in the SS mitochondrial compartment, contribute to the high metabolic efficiency for catch-up fat after caloric restriction and underscore a potential link between diminished skeletal muscle SS mitochondrial energetics, increased ROS concentration, and insulin resistance during catch-up fat., In response to diminished food supply, humans and other mammals can elicit a reduction in energy expenditure, which is partly attributed to an increased metabolic efficiency (1,2). This is viewed [...]

Published
2006

10. A possible link between skeletal muscle mitochondrial efficiency and age-induced insulin resistance

Author

Iossa, Susanna, Mollica, Maria Pina, Lionetti, Lilla, Crescenzo, Raffaella, Tasso, Rosaria, and Liverini, Giovanna

Subjects
Risk factors, Causes of, Diabetes research, Insulin resistance -- Causes of -- Risk factors, Mitochondrial diseases -- Risk factors, Diabetes -- Research
Abstract

Increasing age is associated with obesity and insulin resistance not only in humans but also in rodents (1-5). In fact, ad libitum-fed caged rats are a good animal model that [...], The transition from young to adult age is associated with decreased insulin sensitivity. To investigate whether changes in skeletal muscle mitochondrial function could be involved in the development of insulin resistance, we measured the oxidative capacity and energetic efficiency of subsarcolemmal and intermyofibrillar mitochondria isolated from the skeletal muscle of 60- and 180-day-old rats. Mitochondrial efficiency was tested by measuring the degree of thermodynamic coupling and optimal thermodynamic efficiency, as well as mitochondrial proton leak, which was determined in both the absence (basal) and the presence (fatty acid induced) of palmitate. Serum glucose, insulin, and HOMA index were also measured. The results show that in adult rats, concomitant with increased HOMA index, skeletal muscle mitochondria display higher respiratory capacity and energy efficiency. In fact, thermodynamic coupling and optimal thermodynamic efficiency significantly increased and fatty acid-induced proton leak was significantly lower in the skeletal muscle mitochondria from adult than in younger rats. A deleterious consequence of increased mitochondrial efficiency would be a reduced utilization of energy substrates, especially fatty acids, leading to intracellular triglyceride accumulation and lipotoxicity, thus contributing to the onset of skeletal muscle insulin resistance.

Published
2004

11. Exposure to low doses of p,p’-DDE exerts testicular toxicity in male rats

Author

MIGLIACCIO, VINCENZO, SIMONIELLO, PALMA, PUTTI, ROSALBA, LIONETTI, LILLA', SCUDIERO, ROSARIA, Sica, Raffaela, Universitat de Barcelona, Migliaccio, Vincenzo, Sica, Raffaela, Simoniello, Palma, Putti, Rosalba, Lionetti, Lilla', and Scudiero, Rosaria

Subjects
DDE toxicity, testis, rattus
Published
2016

13. Time-dependent effects on body weight gain and hepatic oxidative stress in rats exposed to both high fat feeding and low doses of persistent organic pollutant

Author

Putti, Rosalba, Sica, Raffaella, Migliaccio, Vincenzo, Pagano, Carmen, Lombardi, Assunta, Lionetti, Lilla', SINU, Putti, Rosalba, Sica, Raffaella, Migliaccio, Vincenzo, C., Pagano, Lombardi, Assunta, and Lionetti, Lilla'

Abstract

Background: Oxidative stress plays an important role into obesity associated metabolic comorbidities. Moreover, exposure to persistent organic pollutants (POPs) is associated with hepatic cellular stress due to detoxification processes. Little is known on the impact associated with chronic simultaneous exposure to both high-fat diet and low doses of persistent organic pollutants, such as p,p´-diphenyldichloroethene (DDE), (DDT’s major metabolite with the highest persistence). Aim: The present work aimed to investigate the effect of different periods of simultaneous exposure to low dose of POP and high-fat feeding on body weight gain and hepatic injury. Given that liver is the main organ involved in response to both high fat diet and toxic injury, we evaluated the development of oxidative stress at the hepatic level. Methods: Three groups of 8 rats were so treated for 4 or 16 weeks: 1) standard diet (10% fat J/J) (N rats); 2) high-fat diet (45% fat J/J) (D rats); 3) high-fat diet plus DDE (10 mg/kg b.w. by gavage) (D+DDE rats). DDE dose used in this work was comparable to the admissible daily intake. Body weight gain and hepatic lipid content were determined. Hepatic oxidative stress was assessed by determining H2O2 production and TBARs content. Results: D rats showed higher body weight gain, hepatic lipid content, H2O2 production and TBARs content compared to control rats after both 4 and 16 weeks. Similar variations were found in D+DDE rats after 4 weeks of treatment. On the other hand, after 16 weeks of treatment D+DDE rats showed lower body weight gain and hepatic lipid content compared to D rats. Moreover, they showed higher H2O2 production and TBARs content compared to D rats. Conclusion: Short period exposure to DDE associated with high fat feeding elicited the same alterations in body weight gain and hepatic oxidative stress found in response to the only exposure to high fat diet. A prolonged period of exposure revealed DDE treatment toxicity as showed by decreased body weight gain and hepatic lipid content and increased oxidative stress.

Published
2014

23. High fat-induced insulin resistance and caveolin 1 activation in visceral adipose tissue: differential effect of high-lard and high-fish oil feeding

Author

Sica, R., Cuomo, T., Piscitelli, E., Cavaliere, G., Odierna, G., Trinchese, G., Gaita, M., De Filippo, C., Mollica, M. P., Putti, R., Lionetti, Lilla', SINU, Sica, Raffaella, T., Cuomo, E., Piscitelli, Cavaliere, Gina, Odierna, Gaetano, Trinchese, Giovanna, M., Gaita, C., De Filippo, Mollica, MARIA PINA, Putti, Rosalba, and Lionetti, Lilla'

Published
2013

24. High-Lard and High-Fish Oil Diets Differ in Their Effects on Insulin Resistance Development, Mitochondrial Morphology and Dynamic Behaviour in Rat Skeletal Muscle

Author

Lionetti, Lilla', Sica, Raffaella, Mollica, MARIA PINA, Gina Cavaliere, Putti, Rosalba, Lionetti, Lilla', Sica, Raffaella, Mollica, MARIA PINA, Cavaliere, Gina, and Putti, Rosalba

Subjects
FIS1, medicine.medical_specialty, high fish oil diet, Insulin, medicine.medical_treatment, MFN2, Skeletal muscle, Biology, Mitochondrion, medicine.disease, high lard diet, medicine.anatomical_structure, Insulin resistance, Endocrinology, mitochondrial fusion, Biochemistry, Internal medicine, medicine, Mitochondrial fission
Abstract

Fish oil (mainly omega 3 polyunsaturated fatty acids), differently from lard (mainly saturated fatty acids) has been suggested to have anti-inflammatory effects associated with amelioration of insulin sensibility. An important role in skeletal muscle insulin resistance development has been recently attributed to mitochondrial dynamic behavior. Mitochondria are dynamic organelles that frequently undergo fission/fusion processes and a shift toward fission process has been associated with skeletal muscle mitochondrial dysfunction and insulin resistance development. The present work aimed to evaluate if the replacement of lard with fish oil in high-fat diet positively affect skeletal muscle mitochondrial dynamic behavior in association with the improvement of insulin-resistance. Body weight gain, systemic insulin-resistance (glucose/insulin ratio), serum TNFα levels and skeletal muscle lipid content were assessed in rats fed a high-lard or high-fish-oil diet for 6 weeks. In skeletal muscle sections, immunohistochemical analysis were performed to detect the presence of insulin receptor substrate 1 (IRS1) and tyrosine phosphorylated IRS1 (key factor in insulin signalling pathway) as well as to detect the main proteins involved in mitochondrial fusion (MFN2 and OPA1) and fission (DRP1 and Fis1) processes. Skeletal muscle mitochondrial ultrastructural features were assessed by electron microscopy. High-fish oil feeding induced lower body weight gain, systemic inflammation and insulin-resistance development as well as skeletal muscle lipid accumulation compared to high-lard feeding. Skeletal muscle sections from high-fish oil fed rats exhibited a greater number of immunoreactive fibers for MFN2 and OPA1 proteins as well as weaker immunostaining for DRP1 and Fis1 compared to sections from high-lard fed rats. Electron microscopy observations suggested a prominent presence of fission events in L rats and fusion events in F rats. The positive effect of the replacement of lard with fish oil in high-fat diet on systemic and skeletal muscle insulin sensibility was associated to changes in mitochondrial dynamic behavior.

Published
2013

28. Effects of endoplasmicum reticulum (ER) stress on insulin action and mitochondrial energy efficiency in skeletal muscle of rats fed with lard or fish oil'

Author

LIONETTI, LILLA', PUTTI, ROSALBA, MOLLICA, MARIA PINA, G. Cavaliere, G. Trinchese, C. De Filippo, G. Gifuni, M. Gaita, A. Pignalosa, I. Donizzetti, A. Barletta, Lionetti, Lilla', Cavaliere, G., Trinchese, G., De Filippo, C., Gifuni, G., Gaita, M., Pignalosa, A., Donizzetti, I., Putti, Rosalba, Barletta, A., and Mollica, MARIA PINA

Published
2012

29. High fat diet-induced hepatic steatosis and insulin-resistance: focus on mitochondrial dynamic behaviour

Author

LIONETTI, LILLA', MOLLICA, MARIA PINA, PUTTI, ROSALBA, I. Donizzetti, R. Sica, A. Pignalosa, G. Gifuni, G. Cavaliere, G. Odierna, M. Gaita, C. De Filippo, G. Trinchese, A. Barletta, Lionetti, Lilla', Mollica, MARIA PINA, Donizzetti, I., Sica, R., Pignalosa, A., Gifuni, G., Cavaliere, G., Odierna, G., Gaita, M., De Filippo, C., Trinchese, G., Barletta, A., and Putti, Rosalba

Published
2012

30. High fat induced hepatic steatosis and mitochondrial dynamic behaviour: time-dependent adaptation

Author

LIONETTI, LILLA', SICA, RAFFAELLA, PUTTI, ROSALBA, Mollica MP, Donizzetti I, Gifuni G, Pignalosa A, Trinchese G, De Filippo C, Gaita M, Cavaliere G, Barletta A, Lionetti, Lilla', Mollica, Mp, Sica, Raffaella, Donizzetti, I, Gifuni, G, Pignalosa, A, Trinchese, G, De Filippo, C, Gaita, M, Cavaliere, G, Barletta, A, and Putti, Rosalba

Abstract

Mitochondria are dynamic organelles that frequently undergo fission and fusion processes, imbalances in which have recently emerged as important etiological factors in obesity and insulin-resistance. The present works aimed to evaluate the association between mitochondrial dynamic behaviour and hepatic steatosis development when rats were fed with high fat diet for different periods. To this end, hepatic lipid accumulation was monitored in rats fed a control diet (10% J/J, N rats) or a high-fat diet (40% J/J, L rats) for 6 or 24 weeks. Mitochondrial fatty acid oxidation rates and the content of fusion (MFN2, OPA1) and fission (DRP1, Fis1) proteins (by western blot and immunohistochemical analysis) were assessed. After 6 weeks, L rats showed increased hepatic lipid accumulation and beta-oxidation associated with a shift toward mitochondrial fission processes (decreased MFN2 content and increased DRP1 and Fis1 content). This fission phenotype, by enhancing mitochondrial surface area, may improve fatty acids intake and, together with the increase in beta-oxidation, may be useful to avoid excessive fat accumulation. After 24 weeks, the further increase in hepatic lipid accumulation was associated with beta-oxidation impairment and a fission phenotype with a decrease in OPA1 content, too. Bearing in mind the role of OPA1 in stabilizing cristae structure and preventing autophagia, its decrease may be useful to eliminate functional impaired mitochondria and minimize cellular damage.

Published
2012

32. Liver mitochondrial function and fusion-fission balance are differently affected by high fat diet rich in lard or fish oil in rat

Author

LIONETTI, LILLA', MOLLICA, MARIA PINA, DONIZZETTI, IMMACOLATA, ODIERNA, GAETANO, PIGNALOSA, ANGELICA, TRINCHESE, GIOVANNA, PUTTI, ROSALBA, G. GIFUNI, R. SICA, G. CAVALIERE, M. GAITA, C. DE FILIPPO, A. BARLETTA, Lionetti, Lilla', Mollica, MARIA PINA, Donizzetti, Immacolata, G., Gifuni, R., Sica, G., Cavaliere, Odierna, Gaetano, Pignalosa, Angelica, Trinchese, Giovanna, M., Gaita, C., DE FILIPPO, A., Barletta, and Putti, Rosalba

Published
2011

33. Development of muscle insulin resistance in rats fed isocaloric high fat diet rich in lard or fish oil: role of skeletal muscle mitochondrial efficiency and oxidative capacity

Author

MOLLICA, MARIA PINA, LIONETTI, LILLA', PIGNALOSA, ANGELICA, TRINCHESE, GIOVANNA, DONIZZETTI, IMMACOLATA, PUTTI, ROSALBA, G. CAVALIERE, G. GIFUNI, M. GAITA, C. DE FILIPPO, R. SICA, S. VERDOLIVA, M. COPPOLA, A. BARLETTA, Mollica, MARIA PINA, Lionetti, Lilla', G., Cavaliere, G., Gifuni, Pignalosa, Angelica, Trinchese, Giovanna, M., Gaita, C., DE FILIPPO, Donizzetti, Immacolata, R., Sica, S., Verdoliva, M., Coppola, Putti, Rosalba, and A., Barletta

Published
2011

36. Effect of chronic overfeeding with high fat diet rich in lard or in fish oil on liver inflammatory parameters in rats

Author

DONIZZETTI, IMMACOLATA, PIGNALOSA, ANGELICA, ODIERNA, GAETANO, MOLLICA, MARIA PINA, LIONETTI, LILLA', PUTTI, ROSALBA, G. Gifuni, G. Cavaliere, C. De Filippo, M. Gaita, R. Aversa, M. Coppola, A. Barletta, I. Soriente, Donizzetti, Immacolata, G., Gifuni, Pignalosa, Angelica, G., Cavaliere, Odierna, Gaetano, C., De Filippo, M., Gaita, Mollica, MARIA PINA, R., Aversa, M., Coppola, A., Barletta, I., Soriente, Lionetti, Lilla', and Putti, Rosalba

Published
2010

37. Obesity and hepatic steatosis development in rats fed high fat diet rich in fish oil or in lard: role of hepatic mitochondrial energy efficiency

Author

M. Gaita, G. Gifuni, G. Cavaliere, C. De Filippo, A. Barletta, PIGNALOSA, ANGELICA, DONIZZETTI, IMMACOLATA, PUTTI, ROSALBA, LIONETTI, LILLA', MOLLICA, MARIA PINA, M., Gaita, Pignalosa, Angelica, G., Gifuni, G., Cavaliere, C., De Filippo, Donizzetti, Immacolata, Putti, Rosalba, A., Barletta, Lionetti, Lilla', and Mollica, MARIA PINA

Published
2010

41. Role of skeletal muscle mitochondria energy efficiency in insulin resistance development in rats fed high fat diet rich in lard or in fish oil

Author

PIGNALOSA, ANGELICA, DONIZZETTI, IMMACOLATA, PUTTI, ROSALBA, MOLLICA, MARIA PINA, LIONETTI, LILLA', M. Gaita, G. Cavaliere, G. Gifuni, C. De Filippo, A. Barletta, Pignalosa, Angelica, M., Gaita, G., Cavaliere, G., Gifuni, Donizzetti, Immacolata, C., De Filippo, A., Barletta, Putti, Rosalba, Mollica, MARIA PINA, and Lionetti, Lilla'

Published
2010

42. Donkey milk and cow milk differently affect ipertriglyceridemia, inflammation and liver mitochondria function

Author

M. Gaita, G. Cavaliere, C. De Filippo, G. Gifuni, D. Neri, R. Aversa, I. Soriente, M. Coppola, A. Barletta, PIGNALOSA, ANGELICA, DI PALO, ROSSELLA, LIONETTI, LILLA', DONIZZETTI, IMMACOLATA, PUTTI, ROSALBA, MOLLICA, MARIA PINA, M., Gaita, G., Cavaliere, C., De Filippo, Pignalosa, Angelica, G., Gifuni, DI PALO, Rossella, D., Neri, Lionetti, Lilla', R., Aversa, Donizzetti, Immacolata, I., Soriente, Putti, Rosalba, M., Coppola, Mollica, MARIA PINA, and A., Barletta

Published
2010

44. EFFECT OF HIGH FAT DIET RICHIN LARD OR IN FISH OIL ON HEPATIC MITOCHONDRIAL OXIDATIVE STRESS AND ENDOPLASMIC RETICULUM (ER) STRESS DURING CHRONIC OVERFEEDING

Author

LIONETTI, LILLA', MOLLICA, MARIA PINA, DONIZZETTI, IMMACOLATA, PIGNALOSA, ANGELICA, PUTTI, ROSALBA, G. GIFUNI, G. CAVALIERE, M. GAITA, C. DE FILIPPO, M. COPPOLA, I. SORIENTE, A. BARLETTA, Lionetti, Lilla', Mollica, MARIA PINA, Donizzetti, Immacolata, G., Gifuni, G., Cavaliere, Pignalosa, Angelica, M., Gaita, C., DE FILIPPO, M., Coppola, I., Soriente, A., Barletta, and Putti, Rosalba

Published
2010

46. Effect of high fat diet rich in lard or fish oil on skeletal muscle insulin resistance

Author

MOLLICA, MARIA PINA, LIONETTI, LILLA', PIGNALOSA, ANGELICA, DONIZZETTI, IMMACOLATA, PUTTI, ROSALBA, C. De Filippo, M. Gaita, G. Cavaliere, G. Gifuni, I. Soriente, M. Coppola, A. Barletta, Mollica, MARIA PINA, Lionetti, Lilla', Pignalosa, Angelica, C., De Filippo, Donizzetti, Immacolata, M., Gaita, G., Cavaliere, G., Gifuni, I., Soriente, M., Coppola, Putti, Rosalba, and A., Barletta

Published
2010

49. From chronic overnutrition to insulin resistance: the role of fat-storing capacity and inflammation. CO-FIRST AUTHOR

Author

LIONETTI, LILLA', MOLLICA, MARIA PINA, LOMBARDI, ASSUNTA, Cavaliere G, Gifuni G, BARLETTA, ANTONIO, Lionetti, Lilla', Mollica, MARIA PINA, Lombardi, Assunta, Cavaliere, G, Gifuni, G, and Barletta, Antonio

Abstract

Aims: We analyze how the inflammatory state in adipose tissue caused by a condition of chronically positive energy balance can lead to insulin resistance first in adipose tissue, then in all insulin-sensitive tissues.Data synthesis: Chronic nutrient overload causes an increase in adipose depots that, if adipose tissue expandability is tow, are characterized by an increased presence of hypertrophic adipocytes. This adipocyte hypertrophy is a possible stress condition for the endoplasmic reticulum (ER) that would lead to a proinflammatory state in adipose tissue. In this condition, ER stress would activate metabolic pathways that trigger insulin resistance, release of macrophage chemoattractant proteins, and in chronic inflammation, the death of the hypertrophic adipocyte. The infiltrated macrophages in turn release inflammatory proteins causing further recruitment of macrophages to adipose tissue and the release of inflammatory cytokines. Following these events, insulin resistance becomes extended to all adipose tissue. Insulin-resistant adipocytes, characterized by low liposynthetic capacity and high lipolytic capacity, cause increased release of free fatty acids (FFA). FFA released by lipolitic adipocytes may also activate Toll-like receptors 4 and then chemokines and cytokines release amplifying insulin resistance, lipolysis and inflammation in all. adipose tissue. Moreover, increased circulating FFA levels, reduced circulating adiponectin levels and leptin resistance lead to decreased lipid oxidation in non-adipose tissues, thereby triggering ectopic accumulation of lipids, lipotoxicity and insulin resistance.Conclusion: All. the conditions that increase circulating fatty acids and cause lipid overloading (obesity, lipoatrophy, lipodystrophy, catabolic states, etc.) induce a lipotoxic state in non-adipose tissues that gives rise to insulin resistance.

Published
2009

50. Insulin resistance development in rats fed high fat diet rich in lard or in fish oil: role of skeletal muscle mitochondria energy efficiency

Author

MOLLICA, MARIA PINA, LIONETTI, LILLA', CAVALIERE, Gina, PIGNALOSA, ANGELICA, DONIZZETTI, IMMACOLATA, PUTTI, ROSALBA, BARLETTA, ANTONIO, M. Gaita, G. Gifuni, C. De Filippo, Mollica, MARIA PINA, Lionetti, Lilla', M., Gaita, Cavaliere, Gina, G., Gifuni, C., De Filippo, Pignalosa, Angelica, Donizzetti, Immacolata, Putti, Rosalba, and Barletta, Antonio

Published
2009

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