Melatonin appears to protect against steroidogenic collapse in both mice fed with high-fat diet and H₂ O₂ -treated...

Area of Science:

• Reproductive Biology
• Endocrinology
• Metabolic Syndrome

Background:

• High-fat diets (HFDs) negatively impact male reproductive health, leading to impaired steroidogenesis and fertility.
• Obesity-associated hypogonadism is a growing concern, necessitating therapeutic interventions.
• Melatonin (MT) is a hormone with antioxidant and anti-inflammatory properties.

Purpose of the Study:

• To investigate the protective effects of melatonin (MT) on testicular dysfunction induced by a high-fat diet (HFD) in male mice.
• To evaluate MT's impact on steroidogenesis, oxidative stress, and endoplasmic reticulum (ER) stress in HFD-fed mice.

Main Methods:

• C57BL/6J male mice were assigned to control (CTRL), HFD, or HFD + MT groups.
• Serum sex hormone levels, testicular protein expression (StAR, P450scc), and markers of oxidative stress (SIRT1, SOD2, GPx4) and ER stress (GRP78, CHOP) were analyzed.
• In vitro studies using TM3 cells assessed MT's protective effects against H2O2-induced steroidogenic dysfunction.

Main Results:

• MT treatment counteracted HFD-induced increases in body weight and adipose tissue.
• Serum sex hormone levels and the expression of testosterone synthesis proteins (StAR, P450scc) were restored by MT.
• MT upregulated antioxidant markers (SIRT1, SOD2, GPx4) and downregulated ER stress markers (GRP78, CHOP), indicating reduced oxidative and ER stress.
• In vitro, MT protected TM3 cells from H2O2-induced damage by enhancing mitochondrial function and reducing stress.

Conclusions:

• Melatonin treatment ameliorates HFD-induced testicular dysfunction in mice by mitigating oxidative and ER stress and restoring steroidogenesis.
• MT supplementation improves hormonal balance and testicular function in the context of HFD-induced obesity.
• Melatonin demonstrates therapeutic potential for managing obesity-associated hypogonadism and male infertility.