Effect of Intermittent Fasting on Lipid Profile, Anthropometric and Hepatic Markers in Non-Alcoholic Fatty Liver Disease (NAFLD): A Systematic Review.

BACKGROUND: The first-line treatment for non-alcoholic fatty liver disease (NAFLD) is lifestyle modification; this should accompany any pharmacological intervention. Intermittent fasting (IF) has shown benefits over metabolic and cardiovascular parameters. Non-religious IF includes Time-Restricted Feeding (TRF), Alternate-Day Fasting (ADF), and 5:2 IF interventions. OBJECTIVE: To evaluate the effects of IF on anthropometric, liver damage, and lipid profile markers in subjects with NAFLD. METHODS: A bibliographic search was carried out according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines using PubMed and Scopus databases. RESULTS: Five studies involving 470 patients with NAFLD were included. In relation to anthropometric markers, all the articles reported body weight reduction (2.48-7.63%), but only ADF and 5:2 IF reported a body weight reduction >5%; also, all the articles reported fat mass reduction. Concerning hepatic markers, all the articles reported a reduction in hepatic steatosis and alanine aminotransferase activity, but no changes in fat-free mass and high-density lipoprotein cholesterol levels. There were variable results on fibrosis, other liver enzymes, waist circumference and body mass index, as well as the levels of triglycerides, total cholesterol, and low-density lipoprotein cholesterol. CONCLUSION: Any form of IF could be potentially beneficial for NAFLD treatment and some associated cardiometabolic parameters. However, it is necessary to evaluate the effects and safety of IF in long-term studies involving a higher number of participants with different stages of NAFLD. The effect of IF on NAFLD-associated vascular risk also needs evaluation.

"Effect of time-restricted feeding on high-fat diet-induced metabolic dysfunction in Drosophila melanogaster".

BACKGROUND: Metabolic alterations associated with obesity have been related to chronodisruption i.e., the desynchronization of molecular clocks that regulate circadian rhythms. The search for tools that improve the dietary treatment of obesity has recently focused on behaviors related to chronodisruption, and intermittent fasting is increasingly gaining interest. Studies in animal models have identified the benefits of time-restricted feeding (TRF) on metabolic alterations associated with changes in circadian rhythms induced by a high-fat diet. We aimed to evaluate the effect of TRF in flies with metabolic damage and chronodisruption. METHODS: Using high-fat diet fed Drosophila melanogaster as a model of metabolic damage and chronodisruption, we determined the impact of 12-h TRF on metabolic and molecular markers. Flies with metabolic dysfunction were switched to a control diet and randomly assigned to Ad libitum or a TRF regimen for seven days. We evaluated total triglyceride content, glycemia, weight, and 24 h mRNA expression rhythms of Nlaz (insulin resistance marker), clock genes (circadian rhythm molecular markers), and the neuropeptide Cch-amide2. RESULTS: Flies with metabolic damage that received TRF showed lower total triglyceride content, Nlaz expression, circulating glucose, and weight compared to Ad libitum. We observed the recovery of some of the high-fat diet-induced alterations in the amplitude of the circadian rhythm, particularly in the peripheral clock. CONCLUSIONS: TRF produced a partial reversal of metabolic dysfunction and chronodisruption of circadian cycles. GENERAL SIGNIFICANCE: TRF could be a useful tool to help to ameliorate metabolic and chronobiologic damage induced by a high-fat diet.

Domeless receptor loss in fat body tissue reverts insulin resistance induced by a high-sugar diet in Drosophila melanogaster.

Insulin resistance is a hallmark of type 2 diabetes resulting from the confluence of several factors, including genetic susceptibility, inflammation, and diet. Under this pathophysiological condition, the dysfunction of the adipose tissue triggered by the excess caloric supply promotes the loss of sensitivity to insulin at the local and peripheral level, a process in which different signaling pathways are involved that are part of the metabolic response to the diet. Besides, the dysregulation of insulin signaling is strongly associated with inflammatory processes in which the JAK/STAT pathway plays a central role. To better understand the role of JAK/STAT signaling in the development of insulin resistance, we used a simple organism, Drosophila melanogaster, as a type 2 diabetes model generated by the consumption of a high-sugar diet. In this model, we studied the effects of inhibiting the expression of the JAK/STAT pathway receptor Domeless, in fat body, on adipose metabolism and glycemic control. Our results show that the Domeless receptor loss in fat body cells reverses both hyperglycemia and the increase in the expression of the insulin resistance marker Nlaz, observed in larvae fed a high sugar diet. This effect is consistent with a significant reduction in Dilp2 mRNA expression and an increase in body weight compared to wild-type flies fed high sugar diets. Additionally, the loss of Domeless reduced the accumulation of triglycerides in the fat body cells of larvae fed HSD and also significantly increased the lifespan of adult flies. Taken together, our results show that the loss of Domeless in the fat body reverses at least in part the dysmetabolism induced by a high sugar diet in a Drosophila type 2 diabetes model.