Laropiprant/Nicotinic Acid

Intermittent fasting is a dietary pattern that encompasses the 5:2 diet, alternate-day fasting, and time-restricted eating. All 3 involve alternating periods of fasting and ad libitum eating. Like other dietary strategies, intermittent fasting typically induces loss of both fat mass and lean mass. Exercise may thus be a useful adjuvant to promote lean mass retention while adding cardiometabolic, cognitive, mental, and emotional health improvements. In this narrative review, we summarize current evidence regarding the combination of intermittent fasting and exercise and its influence on body weight, body composition, cardiometabolic risk, and muscular and cardiorespiratory fitness. A PubMed search was conducted to identify all trials lasting >4 weeks that combined 5:2 diet, alternate-day fasting, or time-restricted eating with any modality exercise and had body weight as an end point. A total of 23 trials (26 publications) were identified. Evidence suggests that combining intermittent fasting with exercise leads to decreased fat mass regardless of weight status. However, evidence is equivocal for the influence on other aspects of weight loss and body composition, fat-free mass, and cardiometabolic risk factors and may be dependent on weight status or exercise doses (ie, frequency, intensity, duration, and modality). Higher-powered trials are needed to determine the efficacy of combining exercise and intermittent fasting for benefits on body weight and cardiometabolic risk. Current evidence suggests that intermittent fasting does not impair adaptation to exercise training, and may improve explosive strength, endurance, and cardiopulmonary measures such as maximal oxygen consumption. In addition, we discuss limitations in the current evidence base and opportunities for continued investigation. Future trials in this area should consider interventions that have increased sample size, longer intervention duration, broadened inclusion criteria, objective measures of diet and exercise adherence, and diversity of sample population.

BDE-209 exposure induced male reproductive toxicity with sperm quality decline. However, the role of autophagy in this was unclear. The purpose was to evaluate the protective effect and its potential mechanism of trehalose (Tre, autophagy inducer) on reproductive damage during spermiogenesis induced by BDE-209. We used 2% w/v Tre and 75 mg/kg/d BDE-209 cotreated mice for 42 days. GC-2 spd cells were cotreated with Tre, chloroquine (CQ, inhibition of autophagic flux), compound C (CC, AMPK inhibitor), and BDE-209. Tre intake significantly recovered decrease in sexual organ ratio and poor sperm quality in BDE-209-exposed mice. Supplementation with Tre rescued sperm head malformation by improving aberrant histone-protamine exchange in BDE-209-exposed mice. However, Tre intake couldn't restore the acrosome biogenesis. In addition, Tre supplementation improved testicular damage induced by BDE-209. BDE-209 blocked autophagic flux with increased P62 and LC3BⅡ/Ⅰ levels. Mechanistically, CQ treatment aggravated elevation of P62 and LC3BⅡ/Ⅰ levels induced by BDE-209, otherwise, CC and Tre treatments inhibited the rise in p-AMPK, p-ULK1, P62 and LC3BⅡ/Ⅰ levels induced by BDE-209. Tre supplementation improved reproductive injury in BDE-209-exposed mice by regulating autophagic flow via AMPK-ULK1 signaling pathways, which providing a new theoretical basis and possible therapeutic targets for male reproductive toxicity.