Daily exposure to bisphenols can affect reproductive functions due to their pseudo-estrogenic and/or anti-androgenic effects. Testicular lipids contain high levels of polyunsaturated fatty acids necessary for sperm maturity, motility, and spermatogenesis. Whether prenatal exposure to bisphenols alters testicular fatty acid metabolism in adult offspring is unknown. Pregnant Wistar rats were gavaged from gestational day 4 to 21 with BPA and BPS (0.0, 0.4, 4.0, 40.0 μg/kg bw/day). Despite increased body and testis weight, the total testicular cholesterol, triglyceride, and plasma fatty acids were unaffected in the offspring. Lipogenesis was upregulated by increased SCD-1, SCD-2, and expression of lipid storage (ADRP) and trafficking protein (FABP4). The arachidonic acid, 20:4 n-6 (ARA) and docosapentaenoic acid, 22:5 n-6 (DPA) levels were decreased in the BPA-exposed testis, while BPS exposure had no effects. The expression of PPARα, PPARγ proteins, and CATSPER2 mRNA were decreased, which are important for energy dissipation and the motility of the sperm in the testis. The endogenous conversion of linoleic acid,18:2 n-6 (LA), to ARA was impaired by a reduced ARA/LA ratio and decreased FADS1 expression in BPA-exposed testis. Collectively, fetal BPA exposure affected endogenous long-chain fatty acid metabolism and steroidogenesis in the adult testis, which might dysregulate sperm maturation and quality.

Background/Objectives: A high-calorie diet contributes to the development of metabolic dysfunction-associated steatotic liver disease (MASLD). Excessive saturated fat intake can lead to metabolic dysfunction, depending on the sources, quality, and duration of the oils and fats consumed. Palmolein, ghee, and coconut oil are common dietary fats that differ in SFA content. The long-term relative metabolic effects of these fats on hepatic steatosis are limited. Methods: Forty adult male C57BL/6 mice were divided into five groups (n=8): chow diet (5% peanut oil) and high-fat (HF) diet (all 25% w/w) enriched with peanut, palmolein, ghee, and coconut oil. All the HF groups are isocaloric and receive 58.4% of their energy from fat. Results: After 6 months, body weight gain and fasting glucose were elevated in all HF groups (p<0.05), except in the peanut-fed group. Ghee-fed mice showed the highest feed efficiency, visceral adiposity, insulin resistance, plasma TG, leptin, liver TG, fatty liver score, IL-6 expression, and malondialdehyde levels (p<0.05). Unlike ghee, coconut oil-fed mice exhibited insulin resistance, hepatic lipid accumulation, and IL-6 expression (p0.05) compared with ghee- and coconut oil-fed groups. Conclusions: Long-term intake of ghee- and coconut oil-enriched diets induces mild microvesicular steatosis and inflammation in the liver compared with the peanut and palmolein diets by triggering insulin resistance and dyslipidemia. The protective effects of palmolein may be due to its tocotrienols, which are known to have hypolipidemic, antioxidant and anti-inflammatory properties.

Background/Objectives: A high-calorie diet contributes to the development of metabolic dysfunction-associated steatotic liver disease (MASLD). Excessive saturated fat intake can lead to metabolic dysfunction, depending on the sources, quality, and duration of the oils and fats consumed. Palmolein, ghee, and coconut oil are common dietary fats that differ in saturated fatty acid (SFA) content. However, the impact of these fats on liver steatosis remains unclear. Methods: Forty adult male C57BL/6 mice were divided into five groups (n = 8/group): chow diet (5% w/w peanut oil) and high-fat diets (HFDs) enriched with peanut, palmolein, ghee, and coconut oil (all 25% w/w). Peanut oil, which is a traditional cooking oil, was used as a reference. All the HFD groups were isocaloric and received 58.4% of their energy from fat. Results: After 6 months, bodyweight gain and fasting glucose were elevated in all HFD-fed groups (p < 0.05), except in the peanut oil-fed group. The ghee-fed group showed the highest feed efficiency, visceral adiposity, insulin resistance, plasma triglycerides (TGs), leptin, liver TGs, fatty liver score, interleukin 6 (IL-6) expression, and TBARS levels (p < 0.05). Unlike the ghee-fed group, the coconut oil-fed group exhibited insulin resistance, hepatic lipid accumulation, and IL-6 expression (p < 0.05), independent of visceral adiposity and oxidative stress. The palmolein oil-fed groups showed minimal changes in fatty liver score (p > 0.05) compared with the ghee- and coconut oil-fed groups. Conclusions: In the HFD setup, chronic intake of ghee- and coconut oil-enriched diets induces microvesicular steatosis and inflammation in the liver compared with the peanut and palmolein diets by triggering insulin resistance and dyslipidemia.