Exercise training performed at the maximal fat oxidation intensity (FMT) stands out as a potential treatment of overweight and obesity. This work is a meta-analysis of randomized clinical trials of studies about the effect of FMT on fat mass and maximal oxygen consumption using PubMed, SCOPUS, EBSCOhost, and ScienceDirect as databases. Two independent reviewers selected 11 trials from 356 publications identified by the following keywords: fatmax, lipoxmax, maximal fat oxidation, peak of fat oxidation, physical training, physical exercise, body fat (BF), fat mass, overweight, and obesity. The risk of bias was assessed following the Cochrane Guidelines. The pooled mean difference was computed for each outcome with the random-effects model and the inverse-variance method. The meta-analysis was performed with the RevMan software v 5.3, and the heterogeneity across studies by the I². The statistical significance was accepted at p < 0.05. Results showed that the FMT reduced body weight (MD = −4.30 kg, p < 0.01, I² = 0%), fat mass (MD = −4.03 kg, p < 0.01, I² = 0%), and waist circumference (MD = −3.34 cm, p < 0.01). Fat-free mass remains unchanged (MD = 0.08 kg, p = 0.85), but maximal oxygen consumption increased (MD = 2.96 mL∙kg⁻¹∙min⁻¹, p < 0.01, I² = 0%). We conclude that FMT at short and medium-term (eight to twenty weeks) reduces body weight and BF, increasing cardiovascular fitness in low physical fitness people with obesity.

Fatty acid translocase/cluster of differentiation 36 (FAT/CD36) is a multifunctional membrane protein activated by a high-fat diet, physical exercise, fatty acids (FAs), leptin, and insulin. The principal function of FAT/CD36 is to facilitate the transport of long-chain fatty acids through cell membranes such as myocytes, adipocytes, heart, and liver. Under high-energy expenditure, the different isoforms of FAT/CD36 in the plasma membrane and mitochondria bind to the mobilization and oxidation of FAs. Furthermore, FAT/CD36 is released in its soluble form and becomes a marker of metabolic dysfunction. Studies with healthy animals and humans show that physical exercise and a high-lipid diet increase FAT/CD36 expression and caloric expenditure. However, several aspects such as obesity, diabetes, Single Nucleotide polymorphisms (SNPs), and oxidative stress affect the normal FAs metabolism and function of FAT/CD36, inducing metabolic disease. Through a comprehensive systematic review of primary studies, this work aimed to document molecular mechanisms related to FAT/CD36 in FAs oxidation and trafficking in skeletal muscle under basal conditions, physical exercise, and diet in healthy individuals.

Previously, we reported that PC12 cells with decreased Dp71 expression (antisense-Dp71 cells) display deficient nerve-growth-factor-induced neurite outgrowth. In this study, we show that disturbed neurite outgrowth of antisense-Dp71 cells is accompanied by decreased adhesion activity on laminin, collagen and fibronectin. In wild-type cells, the immunostaining of Dp71 and β1-integrin overlaps in the basal area contacting the substrate, but staining of both proteins decrease in the antisense-Dp71 cells. Morphology of antisense-Dp71 cells at the electron microscopic level is characterized by the lack of filopodia, cellular projections involved in adhesion. Our findings suggest that Dp71 is required for the efficient PC12 cell attachment to β1-integrin-dependent substrata and that decreased adhesion activity of the antisense-Dp71 cells could determine their deficiency to extend neurites.