N-acetylcysteine in high-sucrose diet-induced obesity: Energy expenditure and metabolic shifting for cardiac health

Novelli, Ethel L. B.; Santos, Priscila P.; Assalin, Heloísa Balan; Souza, Gisele Aparecida; Rocha, Katiucha Karolina Ribeiro; Ebaid, Geovana Xavier; Seiva, Fábio Rodrigues Ferreira; Mani, Fernanda; Fernandes, Ana Angélica Henrique

doi:10.1016/j.phrs.2008.10.004

Cited by 36 publications

(41 citation statements)

References 37 publications

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“…Our real time PCR analysis shows NAC treatment enhanced thermogenic gene expression including Ucp3 , Pgc1α and Dio2 , suggesting that NAC treatment may enhance energy expenditure. Concordant with our results, Novelli et al (15) showed that NAC is able to inhibit carbohydrate oxidation and enhance fat oxidation in rats fed a high-sucrose diet, boosting whole body energy expenditure.…”

Section: Discussionsupporting

confidence: 93%

“…Similar results were obtained in mice subjected to a high cholesterol diet and supplemented with NAC and sesame oil (14). Short-term NAC administration in drinking water prevented high-sucrose induced weight gain and dyslipidemia (15). Collectively, these studies show that NAC is capable of restoring dys-regulated glucose and lipid metabolism, suggesting its potential application in diet-induced obesity, which is closely associated with oxidative stress, inflammation, and metabolic disturbance (16).…”

Section: Introductionmentioning

confidence: 99%

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N-acetylcysteine Protects Mice from High Fat Diet-induced Metabolic Disorders

Gao

Liu

2016

Pharm Res

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Purpose To study the effects of N-acetylcysteine (NAC, C5H9NO3S) on diet-induced obesity and obesity-related metabolic disorders. Methods Six-week-old male C57BL/6 mice fed a chow or high-fat diet (HFD) were treated with NAC (2 g/L) in drinking water for 11 weeks. Its influences on body weight, and food intake were manually measured and on body composition were analyzed by magnetic residence imaging. Glucose meter and ELISA were used to determine serum glucose and insulin levels, and lipid content in the liver. The effects of NAC treatment on mRNA levels of genes involved in inflammation, thermogenesis, and lipid metabolism in various tissues were determined by real time PCR. Results NAC supplementation inhibited the increase of fat mass and the development of obesity when mice were fed an HFD. NAC treatment significantly lowered HFD-induced macrophage infiltration, and enhanced adiponectin gene expression, resulting in reduced hyperglycemia and hyperinsulinemia, and improvement of insulin resistance. NAC oral administration suppressed hepatic lipid accumulation as evidenced by lower levels of triglyceride and cholesterol in the liver. The beneficial effects are associated with a decrease of hepatic Pparγ and its target gene expression, and an increase in the expression of genes responsible for lipid oxidation and activation of farnesoid X receptor. Furthermore, NAC treatment also stimulates expression of thermogenic genes. Conclusion These results provide direct proof of the protective potential of NAC against HFD-induced obesity and obesity-associated metabolic disorders.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

N-acetylcysteine Protects Mice from High Fat Diet-induced Metabolic Disorders

Gao

Liu

2016

Pharm Res

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“…The mechanisms of protection, however, remain obscure [11]. Nutritional and toxicology studies have shown that NAC also improves aerobic glucose metabolism [12], favours glycogenesis [13,14], and reduces insulin resistance [15]. The mechanism behind the improved glycogenesis and its relation to the antioxidative property of NAC is not known and has not been studied in IR models.…”

Section: Introductionmentioning

confidence: 99%

N-acetyl cysteine improves glycogenesis after segmental liver ischemia and reperfusion injury in pigs

Winbladh

Björnsson

Trulsson

et al. 2012

Scandinavian Journal of Gastroenterology

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“…The substrate of lipin-1, phosphatidate, is converted to various phospholipids including cardiolipin, a critical component of mitochondrial membranes [35]. It was reported that NAC reduces the oxidative stress and prevents the metabolic shifting in cardiac tissue, enhancing fatty acid oxidation and reducing anaerobic metabolism in high-sucrose fed conditions [36]. Considering the above information, increased lipin-1 levels with HFD may cause mitochondrial dysfunction in heart, and decreased lipin-1 levels with NAC may have protective effect for heart function.…”

Section: Discussionmentioning

confidence: 99%