Pterostilbene modifies triglyceride metabolism in hepatic steatosis induced by high-fat high-fructose feeding: a comparison with its analog resveratrol

Author(s): S. Gómez-Zorita ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , I. Milton-Laskibar ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , M. T. Macarulla ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , L. Biasutto ⁶ ^, ⁷ ^, ⁸ ^, ⁹ ^, ¹⁰ , A. Fernández-Quintela ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , J. Miranda ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , A. Lasa ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , N. Segues ¹¹ ^, ⁴ ^, ¹² ^, ¹³ ^, ¹⁴ , L. Bujanda ¹¹ ^, ⁴ ^, ¹² ^, ¹³ ^, ¹⁴ , M. P. Portillo ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵

Publication date (Electronic): 2021

Journal: Food & Function

Publisher: Royal Society of Chemistry (RSC)

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Abstract

Mechanisms of action involved in the liver delipidating effects of resveratrol and pterostilbene.

Abstract

The use of phenolic compounds as a new therapeutic approach against NAFLD has emerged recently. In the present study, we aim to study the effect of pterostilbene in the prevention of liver steatosis developed as a consequence of high-fat (saturated) high-fructose feeding, by analysing the changes induced in metabolic pathways involved in triglyceride accumulation. Interestingly, a comparison with the anti-steatotic effect of its parent compound resveratrol will be made for the first time. Rats were distributed into 5 experimental groups and fed either a standard laboratory diet or a high-fat high-fructose diet supplemented with or without pterostilbene (15 or 30 mg per kg per d) or resveratrol (30 mg per kg per d) for 8 weeks. Serum triglyceride, cholesterol, NEFA and transaminase levels were quantified. Liver histological analysis was carried out by haematoxylin–eosin staining. Different pathways involved in liver triglyceride metabolism, including fatty acid synthesis, uptake and oxidation, triglyceride assembly and triglyceride release, were studied. Pterostilbene was shown to partially prevent high-fat high-fructose feeding induced liver steatosis in rats, demonstrating a dose–response pattern. In this dietary model, it acts mainly by reducing de novo lipogenesis and increasing triglyceride assembly and release. Improvement in mitochondrial functionality was also appreciated. At the same dose, the magnitude of pterostilbene and resveratrol induced effects, as well as the involved mechanisms of action, were similar.

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NAFLD is one of the most important causes of liver disease worldwide and will probably emerge as the leading cause of end-stage liver disease in the coming decades, with the disease affecting both adults and children. The epidemiology and demographic characteristics of NAFLD vary worldwide, usually parallel to the prevalence of obesity, but a substantial proportion of patients are lean. The large number of patients with NAFLD with potential for progressive liver disease creates challenges for screening, as the diagnosis of NASH necessitates invasive liver biopsy. Furthermore, individuals with NAFLD have a high frequency of metabolic comorbidities and could place a growing strain on health-care systems from their need for management. While awaiting the development effective therapies, this disease warrants the attention of primary care physicians, specialists and health policy makers.

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Dose translation from animal to human studies revisited.

Shannon Reagan-Shaw, Minakshi Nihal, Nihal Ahmad (2007)

As new drugs are developed, it is essential to appropriately translate the drug dosage from one animal species to another. A misunderstanding appears to exist regarding the appropriate method for allometric dose translations, especially when starting new animal or clinical studies. The need for education regarding appropriate translation is evident from the media response regarding some recent studies where authors have shown that resveratrol, a compound found in grapes and red wine, improves the health and life span of mice. Immediately after the online publication of these papers, the scientific community and popular press voiced concerns regarding the relevance of the dose of resveratrol used by the authors. The animal dose should not be extrapolated to a human equivalent dose (HED) by a simple conversion based on body weight, as was reported. For the more appropriate conversion of drug doses from animal studies to human studies, we suggest using the body surface area (BSA) normalization method. BSA correlates well across several mammalian species with several parameters of biology, including oxygen utilization, caloric expenditure, basal metabolism, blood volume, circulating plasma proteins, and renal function. We advocate the use of BSA as a factor when converting a dose for translation from animals to humans, especially for phase I and phase II clinical trials.