Body fat was significantly different between the groups (P = 0.001). Weight was significantly decreased between the groups at the end of intervention (p = < 0.01). A significant weight reduction was also observed in four groups compared to baseline (p = < 0.01).The control group had significantly higher weight, BMI, WC, BF than subjects received α-LA + Faradic. The α-LA + Faradic group had significantly lower weight, BMI, BF, WC, SLM than faradic and α-LA group. VEGF and NO were not significant in α-LA + Faradic than control.
Sitruin in control, faradic + α-LA groups was higher than α-LA, placebo and faradic group (respectively). PGC in α-LA was higher than control, faradic and in α-LA + Faradic was higher than the control group.
Effect of dietary supplementation to enhance the effects of weight-loss diets has been reported (18, 19).
In line with this study, Huerta et al, found that a-LA supplementation alone or together with EPA lead to weight loss in healthy obese subjects (19). Another study reported that a-LA supplementation in combination with calorie-restricted diet reduced weight, BMI and WC (20). Carbonelli et al. (8) reported that a-LA reduced weight, fat mass and WC only in overweight and obese participants, but not in normal-weight participants. Some Studies found that a-LA reduced weight by decreasing food intake and stimulating energy expenditure (8, 21,22) a-LA could inhibit lipogenesis and adipogenesis, increase lipolysis (23, 24).In contrast with this study, Manning et al, found that a -LA supplementation did not change WC, BMI, Wight compared with placebo (25). Some studies did not report any significant association between weight loss and a -LA supplementation (26, 27). Thereby, the difference between studies could be associated with specific features of the subjects, variety in diet and the duration of treatment.
In our study, Sitruin in α -LA supplementation higher than placebo and α -LA group had higher Sitruin than faradic. These observations are consistent with some studies. Chen et al reported that, α -LA supplementation activated Sitruin and regulated lipid profile (28). α -LA supplementation decreased the acetylation levels of PGC1β by the stimulation of Sitruin (29).
α -LA regulates intrahepatic and serum triglyceride level via the SIRT1 and AMPK signaling pathway (30). α -LA increased NAD+/NADH ratio and activated SIRT1. The SIRT1 is regulated by NAD+, nicotinamide (NA) and the nicotinamide phosphoribosyltransferase (NAMPT). α -LA is converted into dihydrolipoatein by lipoamide dehydrogenase or the thioredoxin reductase enzymes that regulated the NAD+/ NADH ratio. NA can be inhibited SIRT1 and converted to NAD + by NAMPT that it is regulated with deprivation, physical activity and AMPK activation (31).
Dworacka et al reported that α -LA significantly increased VEGF serum levels in diabetic patients (32). α -LA treatment may decrease VEGF serum level. α -LA Supplementation suppressed the VEGF and angiopoietin 2 expression (33, 11).
Another study found that a-lipoic acid combined with exercise significantly decrease BF, WC and hip circumference (34) But α-LA supplementation alone or together with moderate intensity exercise was not change glycemic regulation (34). Razavi et al reported that faradic significantly decreased the abdomen circumference and fat percentage (12).
Chitrav et al reported that faradic stimulated abdominal muscles and reduced abdominal obesity than Interferential Therapy with a supervised exercise program (35). The precise mechanisms of how the faradic stimulation reduced fat mass are unclear. However, Faradic Stimulation breaks down fat molecules and converts them into free fatty acids, which can then enter the Krebs cycle, increasing the muscle atrophy and strength, stimulating the excretion of fluid collected in the organs (34–35).
α -LA affected AMPK hypothalamic, AMPK has a key role in sensing energy and energy bα-LAnce. α -LA has anti-obesity effects by reducing AMPK hypothalamic activity (5). α-LA supplementation by suppressing hypothalamic AMPK may reduce appetite by atypical antipsychotics(5). We found that α-LA by activating AMPK expanded glucose uptake and oxidation of fatty acid in skeletal muscle (5, 6). α -LA is absorbed from the diet and it has anti-obesity properties. α -LA could be suppress hypothalamic AMPK activity, decrease food intake, lipoprotein lipase activity and increased energy expenditure, lipolysis (36).
However, there are some limitations in this study. First, small sample size may affect the generalizability of the results. Weight, body composition, and biochemical indices are influenced by genetic profile. It is possible that differences between the groups were partially induced by gene variations (37, 38). Second, short period of intervention may not be enough to detect the effects of α –LA and Faradic on obesity markers. Third, obesity is a multi-factorial phenotype influencing by many psychological (39) and environmental factors (40). More adjustments should be done in further studies to make a comprehensive conclusion.