S‐Methyl Cysteine Sulfoxide Does Not Ameliorate Weight Gain or Hyperlipidemia in Mice Fed a High‐Fat Diet

Scope Higher intake of cruciferous and allium vegetables is associated with lower cardiometabolic risk. Little research has investigated the cardiometabolic effects of S‐methyl cysteine sulfoxide (SMCSO), found abundant in these vegetables. This study hypothesizes that SMCSO will blunt development of metabolic syndrome features in mice fed high‐fat feed. Methods and results Fifty C57BL/6 male mice are randomly assigned to standard‐chow, high‐fat, or high‐fat supplemented with low‐SMCSO (43 mg kg−1 body weight [BW] day−1), medium‐SMCSO (153 mg kg−1 BW day−1), or high‐SMCSO (256 mg kg−1 BW day−1) for 12‐weeks. High‐fat with SMCSO did not prevent diet‐induced obesity, glucose intolerance, or hypercholesterolemia. Mice fed high‐fat with SMCSO has higher hepatic lipids than mice fed standard‐chow or high‐fat alone. Urinary SMCSO increases at 6‐ and 12‐weeks in the low‐SMCSO group, before reducing 46% and 28% in the medium‐ and high‐SMCSO groups, respectively, at 12‐weeks, suggesting possible tissue saturation. Interestingly, two SMCSO‐fed groups consume significantly more feed, without significant weight gain. Due to limitations in measuring consumed feed, caution should be taken interpreting these results. Conclusion SMCSO (43–256 mg kg−1 BW day−1) does not ameliorate metabolic syndrome features in high‐fat fed mice. Substantial knowledge gaps remain. Further studies should administer SMCSO separately (i.e., gavage), with metabolic studies exploring tissue levels to better understand its physiological action. S‐methyl cysteine sulfoxide (SMCSO) is a sulfur compound abundant in cruciferous (e.g., broccoli) and allium (e.g., onion) vegetables. Adding SMCSO (low, medium, or high) into high fat diets of C57BL/6 male mice over 12‐weeks did not significantly lower the development of metabolic syndrome features. Doses administered were 43 mg/kg, 153 mg/kg, and 256 mg/kg of body weight. These levels of SMCSO are unlikely to attenuate diet‐induced cardiometabolic features in mice.