Aims/hypothesis: Diets rich in n-3 polyunsaturated fatty acids, namely eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), protect against insulin resistance and obesity in rodents and increase insulin sensitivity in healthy humans. We tested whether the anti-diabetic effects of EPA and DHA involve enhanced production of the endogenous insulin sensitiser, adiponectin. Methods: We studied the effects, in an obesity-promoting high-fat diet, of partial replacement of vegetable oils by EPA/DHA concentrate (6% EPA, 51% DHA) over a 5-week period in adult male C57BL/6J mice that either had free access to food or had their food intake restricted by 30%. At the end of the treatment, systemic markers of lipid and glucose metabolism and full-length adiponectin and leptin were measured. Adiponectin (Adipoq) and leptin (Lep) gene expression in dorsolumbar and epididymal white adipose tissue (WAT) and isolated adipocytes was quantified and adipokine production from WAT explants evaluated. Results: In mice with free access to food, plasma triacylglycerols, NEFA, and insulin levels were lower in the presence of EPA/DHA, while glucose and leptin levels were not significantly altered. Food restriction decreased plasma triacylglycerols, glucose, insulin and leptin, but not adiponectin. EPA/DHA increased plasma adiponectin levels, independent of food intake, reflecting the stimulation of Adipoq expression in adipocytes and the release of adiponectin from WAT, particularly from epididymal fat. Expression of Lep and the release of leptin from WAT, while being extremely sensitive to caloric restriction, was unaltered by EPA/DHA. Conclusions/interpretation: Intake of diets rich in EPA and DHA leads to elevated systemic concentrations of adiponectin, largely independent of food intake or adiposity and explain, to some extent, their anti-diabetic effects.

BackgroundSince lifestyle changes are main therapies for non-alcoholic fatty liver disease (NAFLD), changing dietary components (nutritional or bioactive) may play a parallel important role. Few studies have assessed the effects of curcumin on NAFLD (mainly antioxidant and anti-inflammatory effects). We aimed to determine the effects of nano-curcumin (NC) on overweight/obese NAFLD patients by assessing glucose, lipids, inflammation, insulin resistance, and liver function indices, especially through nesfatin.MethodsThis double-blind, randomized, placebo-controlled clinical trial was conducted in the Oil Company Central Hospital, Tehran. 84 overweight/obese patients with NAFLD diagnosed using ultrasonography were recruited according to the eligibility criteria (age 25–50 yrs., body mass index [BMI] 25–35 kg/m2). The patients were randomly divided into two equal NC (n = 42) and placebo (n = 42) groups. Interventions were two 40 mg capsules/day after meals for 3 months. Lifestyle changes were advised. A general questionnaire, a 24-h food recall (at the beginning, middle and end), and the short-form international physical activity questionnaire (at the beginning and end) were completed. Also, blood pressure, fatty liver degree, anthropometrics, fasting blood sugar (FBS) and insulin (FBI), glycated hemoglobin (HbA1c), homeostasis model assessment-insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), tumor necrosis factor-alpha (TNF-α), high sensitive c-reactive protein (hs-CRP), interleukin-6 (IL-6), liver transaminases, and nesfatin were determined at the beginning and end.ResultsNC compared with placebo significantly increased HDL, QUICKI, and nesfatin and decreased fatty liver degree, liver transaminases, waist circumference (WC), FBS, FBI, HbA1c, TG, TC, LDL, HOMA-IR, TNF-α, hs-CRP, and IL-6 (P < 0.05). The mean changes in weight, BMI, body composition (BC), and blood pressure were not significant (P > 0.05). After adjustment for confounders, the changes were similar to the unadjusted model.ConclusionNC supplementation in overweight/obese NAFLD patients improved glucose indices, lipids, inflammation, WC, nesfatin, liver transaminases, and fatty liver degree. Accordingly, the proposed mechanism for ameliorating NAFLD with NC was approved by the increased serum nesfatin and likely consequent improvements in inflammation, lipids, and glucose profile. Further trials of nano-curcumin’s effects are suggested.Trial registrationIranian Registry of Clinical Trials, IRCT2016071915536N3. Registered 2016-08-02.

At the end of 2019, a novel flu‐like coronavirus named COVID‐19 (coronavirus disease 2019) was recognized by World Health Organization. No specific treatments exist for COVID‐19 at this time. New evidence suggests that therapeutic options focusing on antiviral agents may alleviate COVID‐19 symptoms as well as those that lead to the decrease in the inflammatory responses. Flavonoids, as phenolic compounds, have attracted considerable attention due to their various biological properties. In this review, the promising effects and possible mechanisms of action of naringenin, a citrus‐derived flavonoid, against COVID‐19 were discussed. We searched PubMed/Medline, Science direct, Scopus, and Google Scholar databases up to March 2020 using the definitive keywords. The evidence reviewed here indicates that naringenin might exert therapeutic effects against COVID‐19 through the inhibition of COVID‐19 main protease, 3‐chymotrypsin ‐ like protease (3CLpro), and reduction of angiotensin converting enzyme receptors activity. One of the other mechanisms by which naringenin might exert therapeutic effects against COVID‐19 is, at least partly, by attenuating inflammatory responses. The antiviral activity of the flavanone naringenin against some viruses has also been reported. On the whole, the favorable effects of naringenin lead to a conclusion that naringenin may be a promising treatment strategy against COVID‐19.

Ulcerative colitis (UC) is a chronic recurrent inflammation of the colon. It has been proposed that the UC pathogenesis may be related to vitamin D deficiency and/or vitamin D administration in UC patients may have an ameliorating effect on the intestinal inflammation. The aim of this study was to assess the effect of vitamin D on the serum levels of immune cytokines in UC patients. In this double‐blind randomized controlled trial, 90 mild‐to‐moderate UC patients were assigned to get either a single muscular injection of 7.5 mg vitamin D3 or 1 mL normal saline as placebo. Three months later serum levels of IL‐4, IL‐10, IL‐12p70, IFN‐γ, and TNF‐α were measured. Two group variables were compared using independent t‐test and analysis of covariance (ANCOVA). There was a significant increase in vitamin D only in the vitamin D group. Compared to placebo, vitamin D had significant decreasing effects on serum TNF‐α, IFN‐γ, and IL12p70 levels, but it had no significant effect on serum levels of IL4 and IL10. Vitamin D seems to inhibit Th1 immune responses and have no effect on Th2 responses. The findings of this study support several in vitro studies, which suggest a therapeutic immunomodulatory potential of vitamin D.

Observational studies suggest better clinical outcomes following critical illness in patients with overweight and obesity (obesity paradox). An understanding of the morphologic, physiologic and metabolic changes in adipose tissue in critical illness may provide an explanation. Recent studies have demonstrated the transformation of white to brown-like adipocytes due to the "browning process," which has been of interest as a potential novel therapy in obesity during the last decade. The characteristics of the browning of white adipose tissue (WAT) include the appearance of smaller, multilocular adipocytes, increased UCP1 mRNA expression, mitochondrial density and respiratory capacity. These changes have been identified in some critical illnesses, which specifically refers to burns, sepsis and cancer cachexia in this study. The pathophysiological nature of WAT browning, underlying mechanisms, main regulators and potential benefits and harms of this process are interesting new areas that warrants further investigations. In this review, we discuss emerging scientific discipline of adipose tissue physiology in metabolic stress, available data, gaps of knowledge and future perspectives. Future investigations in this field may provide insights into the underlying mechanisms and clinical aspects of browning that may further our understanding of the proposed obesity paradox following critical illness, which may in turn open up opportunities for novel therapies to save lives and improve recovery.