Effect of vitamin C supplementation on the development of metabolic syndrome in male Swiss mice
DOI:
https://doi.org/10.34117/bjdv11n4-058Keywords:
metabolic syndrome, MSG, vitamin C, nitric oxide, cardiovascular parametersAbstract
Modern lifestyles-characterized by poor diet, sedentary behavior, and stress-are linked to chronic diseases such as heart disease, diabetes, and metabolic syndrome (MetS). MetS is defined by a cluster of cardiovascular risk factors, including hypertension, hyperglycemia, and dyslipidemia (elevated LDL and reduced HDL), often associated with insulin resistance. Recent studies have explored the protective effects of antioxidant supplementation, including vitamin C, on MetS. However, its therapeutic use remains debated, warranting further investigation. This study aimed to evaluate the effects of oral vitamin C supplementation on the development of MetS induced by monosodium glutamate (MSG) in neonatal Swiss mice. Newborns received subcutaneous MSG (4 mg/g body weight) or saline for five days. At 30 days of age, male mice were assigned to six groups (n =10/group): MSG-CTL (untreated), MSG-Vit.C (vitamin C treated), MSG-water (water treated), SAL-CTL (saline control), SAL-Vit.C, and SAL-water. MS development was assessed by measuring blood pressure, Lee index, and blood glucose levels. At the end of treatment, plasma nitric oxide (NO) levels, cardiovascular parameters, and adiposity were evaluated. MSG-treated mice showed increased Lee index, hypertension, and hyperglycemia compared to saline controls. Vitamin C supplementation prevented these alterations, maintaining physiological parameters similar to health controls. Additionally, vitamin C significantly reduced visceral fat accumulation and NO production. These findings suggest that vitamin C may exert a protective effect against MetS and support its potential as a preventive strategy in metabolic disorders.
References
AKOLKAR, G. et al. Doxorubicin-induced nitrosative stress is mitigated by vitamin C via the modulation of nitric oxide synthases. American Journal of Physiology-Cell Physiology, v. 312, n. 4, p. C418–C427, 2017.
ALTATHER, W. et al. Neonatal exposure to monosodium glutamate results in impaired auditory brainstem structure and function. Hearing Research, v. 405, p. 108243, 2021.
BERNARDIS, L.; PATTERSON, B. Correlation between 'Lee index' and carcass fat content in weanling and adult female rats with hypothalamic lesions. Journal of Endocrinology, v. 40, n. 4, p. 527–528, 1968.
BILBIS, L. et al. Effect of vitamins A, C, and E supplementation in the treatment of metabolic syndrome in albino rats. BioMed Research International, v. 2012, p. 678582, 2012.
BOVOLINI, A. et al. Metabolic syndrome pathophysiology and predisposing factors. International Journal of Sports Medicine, v. 42, n. 03, p. 199–214, 2021.
BURDE, R.; SCHAINKER, B.; KAYES, J. Acute effect of oral and subcutaneous administration of monosodium glutamate on the arcuate nucleus of the hypothalamus in mice and rats. Nature, v. 233, n. 5314, p. 58–60, 1971.
CARR, A. C.; MAGGINI, S. Vitamin C and immune function. Nutrients, v. 9, n. 11, p. 1211, 2017.
CHO, Y.; LEE, S. Y. Useful biomarkers of metabolic syndrome. International Journal of Environmental Research and Public Health, v. 19, p. 15003, 2022.
CUNHA, N. et al. Cox-2 inhibition attenuates cardiovascular and inflammatory aspects in monosodium glutamate-induced obese rats. Life Sciences, v. 87, n. 11–12, p. 375–381, 2010.
DAS, U. N. Vitamin C for type 2 diabetes mellitus and hypertension. Archives of Medical Research, v. 50, n. 2, p. 11–14, 2019.
DU, W. et al. Effect of flavonoids in hawthorn and vitamin C prevents hypertension in rats induced by heat exposure. Molecules, v. 27, n. 3, p. 866, 2022.
FERNÁNDEZ-SÁNCHEZ, A. et al. Inflammation, oxidative stress, and obesity. International Journal of Molecular Sciences, v. 12, n. 5, p. 3117–3132, 2011.
GARCIA-DIAZ, D. F. et al. Vitamin C in the treatment and/or prevention of obesity. Journal of Nutritional Science and Vitaminology, v. 60, n. 6, p. 367–379, 2014.
HUTCHESON, R.; ROCIC, P. The metabolic syndrome, oxidative stress, environment, and cardiovascular disease: the great exploration. Journal of Diabetes Research, v. 2012, p. 271028, 2012.
KOLB, H. Obese visceral fat tissue inflammation: from protective to detrimental? BMC Medicine, v. 20, n. 1, p. 494, 2022.
LOPES, F. N. C. et al. Antioxidant therapy reverses sympathetic dysfunction, oxidative stress, and hypertension in male hyperadipose rats. Life Sciences, v. 295, p. 120405, 2022.
LUCCHETTI, B. F. C. et al. Metabolic syndrome aggravates cardiovascular, oxidative and inflammatory dysfunction during the acute phase of Trypanosoma cruzi infection in mice. Scientific Reports, v. 9, n. 1, p. 18885, 2019.
MAYER, C. M.; BELSHAM, D. D. Central insulin signaling is attenuated by long-term insulin exposure via insulin receptor substrate-1 serine phosphorylation, proteasomal degradation, and lysosomal insulin receptor degradation. Endocrinology, v. 151, n. 1, p. 75–84, 2010.
MCCRACKEN, E.; MONAGHAN, M.; SREENIVASAN, S. Pathophysiology of the metabolic syndrome. Clinics in Dermatology, v. 36, n. 1, p. 14–20, 2018.
NAKAMA, R. P. et al. Metabolic syndrome induces benefits in mice experiencing severe sepsis, comparable to the effects of low-dose aspirin pretreatment in septic mice lacking metabolic syndrome. Immunology, v. 139, p. 112694, 2024.
NAKAMA, R. P. et al. Metabolic syndrome improves cardiovascular dysfunction and survival during cecal ligation and puncture-induced mild sepsis in mice. Life Sciences, v. 286, p. 120033, 2021.
NOSRATABADI, S. et al. The effects of vitamin C supplementation on glycemic control in patients with type 2 diabetes: A systematic review and meta-analysis. Diabetes Research and Clinical Practice, v. 17, n. 8, p. 102824, 2023.
NOUBIAP, J. J. et al. Geographic distribution of metabolic syndrome and its components in the general adult population: A meta-analysis of global data from 28 million individuals. Diabetes Research and Clinical Practice, v. 188, p. 109924, 2022.
OLNEY, J. W. Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate. Science, v. 164, n. 3880, p. 719–721, 1969.
ROBERTS, C. K.; SINDHU, K. K. Oxidative stress and metabolic syndrome. Life Sciences, v. 84, n. 21–22, p. 705–712, 2009.
SAKLAYEN, M. G. The global epidemic of the metabolic syndrome. Current Hypertension Reports, v. 20, n. 2, p. 1–8, 2018.
SCULLY, T. et al. Obesity, type 2 diabetes, and cancer risk. Frontiers in Oncology, v. 10, p. 615375, 2021.
UENO, M. et al. Regulation of insulin signalling by hyperinsulinaemia: role of IRS-1/2 serine phosphorylation and the mTOR/p70 S6K pathway. Diabetologia, v. 48, p. 506–518, 2005.
ZHANG, Y.; ZHANG, D.-Z. Associations of vegetable and fruit consumption with metabolic syndrome. A meta-analysis of observational studies. Public Health Nutrition, v. 21, n. 9, p. 1693–1703, 2018.

