Experimental animal studies investigating the effects of high-sugar and metabolically adverse diets on testosterone regulation and male reproductive outcomes.
| Study | Animal model | Diet composition | Dose/Exposure mode | Duration | Testosterone outcome | Testicular/Reproductive outcome |
|---|---|---|---|---|---|---|
| Tkachenko et al., 2020 [17] | Juvenile male Wistar rats | 10% fructose drinking solution (~100 g/L) with standard pellet chow | Ad libitum fructose solution replacing drinking water | 60 days (juvenile → pubertal transition) | ↓Serum testosterone with compensatory ↑LH and FSH (ELISA-based measurement) | Seminiferous epithelial degeneration, reduced spermatogenesis index, ↓epididymal sperm count, impaired fertilising capacity |
| Hsia et al., 2022 [21] | Adolescent male Sprague-Dawley rats | High-fructose diet (65% fructose chow) vs. standard diet | Ad libitum high-fructose feeding | 21 weeks (chronic exposure) | ↓Plasma and Leydig cell testosterone production (RIA-based measurement) | Impaired LH/cAMP-PKA signaling responsiveness, reduced steroidogenic capacity in isolated Leydig cells, ↓sperm vitality with metabolic dysregulation (hyperinsulinemia, hyperglycemia) |
| Sertorio et al., 2022 [22] | Male Wistar rat offspring | HFHS diet (32% fat; 50% carbohydrates with ~25% from sugar; sweetened condensed milk source) vs. control diet | Ad libitum parental dietary exposure (paternal preconception + maternal gestation/lactation) followed by offspring standard diet | 10 weeks paternal exposure + gestation/lactation programming; offspring evaluated at 90 days | ↓Serum testosterone (chemiluminescence assay) with reduced expression of steroidogenic genes (StAR, Hsd17b3) | Testicular inflammation (↑cytokines), oxidative stress, impaired spermatid number and sperm morphology, and altered epigenetic regulatory markers |
| Jing et al., 2020 [13] | Adult male C57BL/6J mice + primary rat Leydig cells/TM3 Leydig cell line | HFD (34.9% fat; 26.3% carbohydrate) vs. standard diet | Ad libitum high-fat feeding; mechanistic in-vitro oxLDL exposure (25–100 µg/mL) | 16 weeks (chronic metabolic exposure) | ↓Serum testosterone and reduced Leydig cell steroidogenesis (ELISA-based hormone measurement) | oxLDL accumulation via CD36 signaling, mitochondrial dysfunction (↓respiratory complex activity, ↓ATP), ↑ROS production and MAPK activation, reduced expression of steroidogenic proteins (StAR, P450scc, 3β-HSD, 17β-HSD), impaired sperm motility and count |
| Suleiman et al., 2020 [14] | Adult male Sprague-Dawley rats (obesity model) | HFD: 68 g standard chow + 32 g ghee + 12% cholesterol (energy-dense obesogenic diet) vs. standard diet | Ad libitum high-fat feeding | 12 weeks (chronic exposure) | ↓Serum and intra-testicular testosterone; altered LH and FSH levels | ↓Expression of steroidogenic genes (StAR, CYP11A1, 3β-HSD, 17β-HSD), ↑oxidative stress in epididymal tissue, impaired sperm motility, viability, and morphology, reduced Leydig cell number, and spermatogenic disruption |
ATP: adenosine triphosphate; CD36: cluster of differentiation 36; CYP11A1: cholesterol side chain cleavage enzyme; ELISA: enzyme-linked immunosorbent assay; FSH: follicle-stimulating hormone; HFD: high-fat diet; HFHS: high-fat high-sugar; HSD: hydroxysteroid dehydrogenase; LH: luteinizing hormone; MAPK: mitogen-activated protein kinase; oxLDL: oxidized low-density lipoprotein; RIA: radioimmunoassay; ROS: reactive oxygen species; StAR: steroidogenic acute regulator.