This review deals with the relationship among nutrition, the immune system, and coronavirus disease 2019 (COVID-19). The influence of nutrients and bioactive molecules present in foodstuffs on immune system activity, the influence of COVID-19 on the nutritional status of the patients, and the dietary recommendations for hospitalized patients are addressed. Deficient nutritional status is probably due to anorexia, nausea, vomiting, diarrhea, hypoalbuminemia, hypermetabolism, and excessive nitrogen loss. There is limited knowledge regarding the nutritional support during hospital stay of COVID-19 patients. However, nutritional therapy appears as first-line treatment and should be implemented into standard practice. Optimal intake of all nutrients, mainly those playing crucial roles in immune system, should be assured through a diverse and well-balanced diet. Nevertheless, in order to reduce the risk and consequences of infections, the intakes for some micronutrients may exceed the recommended dietary allowances since infections and other stressors can reduce micronutrient status. In the case of critically ill patients, recently published guidelines are available for their nutritional management. Further, several natural bioactive compounds interact with the angiotensin-converting enzyme 2 (ACE2) receptor, the gateway for severe acute respiratory syndrome (SARS) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Natural bioactive compounds can also reduce the inflammatory response induced by SARS-CoV-2. These compounds are potential beneficial tools in the nutritional management of COVID-19 patients.
Non-alcoholic fatty liver disease (NAFLD) is one of the most common manifestations of chronic liver disease worldwide. The aim of the present study was to assess the effect of resveratrol on liver fat accumulation, as well as on the activity of those enzymes involved in lipogenesis and fatty acid oxidation in fa/fa Zucker rats. A total of thirty rats were assigned to three experimental groups and orally treated with resveratrol for 6 weeks, or without resveratrol (C: control group; RSV15 group: 15 mg/kg body weight per d; RSV45 group: 45 mg/kg body weight per d). Liver histological analysis was performed by microscopy. Levels of hepatic carnitine palmitoyltransferaseIa (CPT-Ia), acyl-coenzyme A oxidase (ACO), fatty acid synthase, glucose-6-phosphate dehydrogenase and malic enzyme were assessed by spectrophotometry, and acetyl-CoA carboxylase was assessed by radiometry. Commercial kits were used to determine serum TAG, NEFA, total HDL and non-HDL-cholesterol, glycerol, ketonic bodies, glucose, insulin, adiponectin, aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP), hepatic TAG, thiobarbituric acid reactive substrates, GSH (GSSG) and superoxide dismutase. Resveratrol reduced liver weight and TAG content. It did not modify the activity of lipogenic enzymes but it did increase CPT-Ia and ACO activities. NEFA and ALP were reduced in both resveratrol-treated groups. AST/GOT was reduced only by the lowest dose. ALT/GPT, TAG and adiponectin remained unchanged. Resveratrol reduced liver oxidative stress. This study demonstrates that resveratrol can protect the liver from NAFLD by reducing fatty acid availability. Moreover, resveratrol also protects liver from oxidative stress.
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