|
| |
 |
|
| REVIEW ARTICLE |
|
| Year : 2022 | Volume
: 8
| Issue : 2 | Page : 86-89 |
|
Antioxidants and its role in endocrine disorders
Urvashi Midha, Juhi Aggarwal, Jyoti Batra, Eram Hussain Pasha, Luna Sinha
Department of Biochemistry, Santosh Medical College and Hospital, Santosh Deemed to be University, Ghaziabad, Uttar Pradesh, India
| Date of Submission | 24-Nov-2022 |
| Date of Acceptance | 24-Nov-2022 |
| Date of Web Publication | 11-Jan-2023 |
Correspondence Address:
Juhi Aggarwal
Department of Biochemistry, Santosh Medical College and Hospital, Santosh Deemed to be University, Ghaziabad - 201 009, Uttar Pradesh
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/sujhs.sujhs_38_22
An excessive synthesis of ROS results in oxidative stress and results in deleterious process that damages cell structures i.e. lipids, proteins, and DNA. Oxidative stress plays a major role in various human disease states, including endocrine dysfunction. A number of diseases connected with free radicals have recently been reported in the medical field. The risk of diseases caused by oxidative stress is exacerbated by an unhealthy lifestyle, chemical exposure, pollution, cigarette smoking, drugs, illness, and stress, among other things. Antioxidants are molecules that can scavenge free radicals and aid in the reduction of oxidative stress-induced damage. Traditional herbal treatments and dietary items were the primary sources of antioxidants for ancient peoples, protecting them from free radical damage. In this article, we present a brief overview of the role of oxidative stress in a variety of common human endocrine disorders, such as diabetes and thyroid disease, as well as a discussion of the therapeutic potential of dietary antioxidant (Vitamin C & Vitamin A) techniques.
Keywords: Antioxidants, diabetes mellitus, oxidative stress, reactive oxygen species
How to cite this article:
Midha U, Aggarwal J, Batra J, Pasha EH, Sinha L. Antioxidants and its role in endocrine disorders. Santosh Univ J Health Sci 2022;8:86-9 |
How to cite this URL:
Midha U, Aggarwal J, Batra J, Pasha EH, Sinha L. Antioxidants and its role in endocrine disorders. Santosh Univ J Health Sci [serial online] 2022 [cited 2023 May 30];8:86-9. Available from: http://www.sujhs.org/text.asp?2022/8/2/86/367573 |
| Introduction | |  |
Reactive oxygen species (ROS) and reactive nitrogen species are the by-products resulting from the cellular redox process. These reactive species play a dual role in humans as both toxic and beneficial compounds. The delicate balance between their two opposite effects is undoubtedly a key aspect of life. At low or moderate levels, reactive species exert beneficial effects on cellular redox signaling and immune function, but at high concentrations, they produce oxidative stress, a harmful process that can damage cell function and structures.[1],[2]
Free radicals are generally eliminated by the body's effective mechanisms, which include antioxidant enzymes (superoxide dismutase [SOD], catalase, and glutathione peroxidase) and nutrient-derived antioxidant small molecules (Vitamin E, Vitamin C, carotenes, flavonoids, glutathione, uric acid, and taurine). A delicate balance exists between free radicals and antioxidants in healthy humans. Oxidative stress causes antioxidant levels to fall below normal in several pathologic circumstances, such as diabetes and critically ill patients. Antioxidant supplements are believed to be beneficial in such cases. An antioxidant refers to any molecule capable of stabilizing or deactivating free radicals before they attach to cells. Humans have evolved highly complex antioxidant systems (enzymic and nonenzymic), which work synergistically, and in combination with each other to protect cells and organ systems of the body against free radical damage. Antioxidants can be endogenously produced substances or be obtained from exogenous sources, for example, as a part of a diet or as dietary supplements. Some dietary compounds that do not neutralize free radicals, but enhance endogenous activity can also be classified as antioxidants.[3]
| Antioxidants in Thyroid Disorders | | |
Vitamin C improves anomalies in serum-free T4, T3, and thyroid-stimulating hormone concentrations in patients with hypothyroidism and gastrointestinal disease. This method is beneficial in the treatment of these patients.
Ascorbic acid is a nonenzymatic antioxidant water-soluble material that, like Vitamin E, does not accumulate in cell membrane properties and is usually found inside and outside cells. However, cases of poisoning caused by excessive supplement consumption have not been reported, except for reduction, which is dissolved by removing ascorbic acid from the diet.[4]
Among the endocrine gland, the thyroid gland is located in the neck near the larynx and due to secretion and production of specific elements and substances have particular importance. Effective hormones on thyroid gland metabolism are T4 and T3. T4 or thyroxin has important metabolic functions in the body, such as increased oxygen consumption by cells, glycolysis or glucose uptake, regulation of heart rate efficiency, and effect on fat metabolism.[5],[6],[7],[8],[9],[10] According to some researches, ascorbic acid with its antioxidant effect prevents tissue damage from free radicals and finally prevents from tissue damage and destruction.[5],[6],[11]
Vitamin A is required by the body for a number of key metabolic tasks, including vision, immune function modulation, growth, and development.[12] Vitamin A is not a well-known antioxidant, and only a few studies have suggested that it may have an antioxidant impact. All-trans retinoic acid, on the other hand, has been shown to have an important role in limiting hepatic stellate cell activation by regulating thioredoxin-interacting protein and lowering oxidative stress levels.[13] Furthermore, in both healthy and varicocele sperm, all-trans retinoic acid was found to increase SOD and glutathione S-transferase activities while decreasing malondialdehyde and ROS.[14] Therefore, there is growing evidence suggesting that Vitamin A enhances antioxidant enzyme activities and may play a role in protecting the body against oxidative stress damage.
The transport of Vitamin A in plasma is a distinct process mediated by plasma retinol-binding protein 4 (RBP4), which is mainly produced by hepatocytes.[15] RBP4 forms a reversible complex with a carrier protein called transthyretin (TTR). RBP4 binding to TTR prevents the extensive loss of RBP4 through glomerular filtration.[6]
It has been known that Vitamin A deficiency affects thyroid hormones for many years, resulting in iodine deficiency disorders, whereas Vitamin A supplementation alleviates the risk of subclinical hypothyroidism.[16],[17] Recently, a study has been conducted to investigate the relationship between Vitamin A and thyroid function in obese individuals. Vitamin A deficiency is more common in subjects with obesity and is significantly related to thyroid dysfunction. Adequate Vitamin A levels improved thyroid function in obese subjects with subclinical hypothyroidism.[18]
| Antioxidants in Diabetes | | |
Type 2 diabetes mellitus (T2DM) is a chronic noncommunicable disease characterized by early insulin resistance, late islet β-cell failure, and hyperglycemia, accounting for 90% of diabetic patients.[19]
Diabetes is one of the world's most common chronic diseases. Diabetes incidence has gradually increased in recent years, owing to continual improvements in people's living standards and changes in dietary structure. Ascorbic acid supplementation has been demonstrated in studies to lower blood glucose, boost insulin synthesis and secretion, improve insulin resistance, and minimize the occurrence and progression of type 2 diabetes complications.
Ascorbic acid, also known as Vitamin C, is an effective water-soluble antioxidant, which has a scavenging effect on excessive free radicals in the body of diabetic patients and a protective effect on tissue damage caused by oxidative stress.[20],[21] Some studies have found that ascorbic acid supplementation can improve islet cell function in patients with T2DM, which can be used for the early prevention of diabetes and the later treatment of complications.[22],[23] Furthermore, some studies,[24] but not others, have shown that ascorbic acid supplementation can regulate fasting blood glucose and glycosylated hemoglobin A1c and improve insulin resistance.
Vitamin A is a class of unsaturated nutritional organic substances that comprises the carotenoids retinol, retinal, retinoic acid, and provitamin A carotenoids. Carotene, the most frequent form of carotene in plants, is a precursor to Vitamin A in nature, where it is activated by beta-carotene 15, 15'-monooxygenase in the small intestine and liver. The fundamental form of Vitamin A found in animal-source foods is ester-retinyl palmitate, which is decertified in the small intestines to alcohol-retinol.
Vitamin A is a vitamin that is essential for many physiological functions; however, its role in glucose metabolism is not well understood. Rat studies have revealed a link between glycogen concentration in the liver and Vitamin A levels.[25],[26]
Feeding rodents with a Vitamin A-deficient diet altered the structure and functions of the pancreas by diminishing the islet cells, possibly by inducing cellular stress-mediated apoptosis and reducing stearoyl-CoA desaturase 1 (SCD1)-mediated oleic acid (C18:1) synthesis. It resulted in decreased levels of plasma insulin, glucagon, and C-peptide and perturbed the overall cellular metabolism.[27] Experimental studies have also shown that maternal deficiency of Vitamin A during pregnancy affects offspring and leads to a decrease in β-cell functions by reducing fetal β-cell replication and impairing glucose-stimulated insulin secretion.[28],[29]
Recently, much attention has been devoted to the role of Vitamin A in the regulation of macronutrient metabolism in various disease states, especially obesity, type 2 diabetes, and other metabolic disorders. Vitamin A is one of the antioxidant factors; hence, the limits of its concentration in the body may play a role in the development of diabetes.[30],[31]
| Conclusion | | |
Thyroid hormones reacted to antioxidants to avoid the onset of certain disorders in the thyroid gland by shielding the biological system from potentially damaging effects of processes or reactions that can cause excessive oxidation. Even while vitamins have significant impacts on the risk of diabetes mellitus, as well as its progression and consequences, there is in most situations insufficient evidence to recommend individual or multivitamin supplementation in the general diabetic population. To ensure an acceptable nutritional status, the best recommendation should be to consume suitable quantities of those foods that contain vitamins in sufficient levels. In this regard, nutritional evaluations are required to identify particular intake inadequacies and make recommendations.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Pham-Huy LA, He H, Pham-Huy C. Free radicals, antioxidants in disease and health. Int J Biomed Sci 2008;4:89-96.  |
| 2. | Sen S, Chakraborty R, Sridhar C, Reddy YS, De B. Free radicals, antioxidants, Diseases and phytomedicines: Current status and Future prospect. Int J Pharma Sci Rev Res 2010;3:91-100. |
| 3. | Sen S, Chakraborty R. The role of antioxidants in human health. In: Andreescu S, Hepeleditors M, editors. ACS Symposium Series. Vol. 1083. Washington, DC: American Chemical Society; 2011. p. 1-37. |
| 4. | Abahusain MA, Wright J, Dickerson JW, de Vol EB. Retinol, alpha-tocopherol and carotenoids in diabetes. Eur J Clin Nutr 1999;53:630-5. |
| 5. | Kotnik P, Fischer-Posovszky P, Wabitsch M. RBP4: A controversial adipokine. Eur J Endocrinol 2011;165:703-11. |
| 6. | Pullakhandam R, Palika R, Ghosh S, Reddy GB. Contrasting effects of type 2 and type 1 diabetes on plasma RBP4 levels: The significance of transthyretin. IUBMB Life 2012;64:975-82. |
| 7. | Wolf G. Serum retinol-binding protein: A link between obesity, insulin resistance, and type 2 diabetes. Nutr Rev 2007;65:251-6. |
| 8. | van Hoek M, Dehghan A, Zillikens MC, Hofman A, Witteman JC, Sijbrands EJ. An RBP4 promoter polymorphism increases risk of type 2 diabetes. Diabetologia 2008;51:1423-8. |
| 9. | Erikstrup C, Mortensen OH, Nielsen AR, Fischer CP, Plomgaard P, Petersen AM, et al. RBP-to-retinol ratio, but not total RBP, is elevated in patients with type 2 diabetes. Diabetes Obes Metab 2009;11:204-12. |
| 10. | Zatalia SR, Sanusi H. The role of antioxidants in the pathophysiology, complications, and management of diabetes mellitus. Acta Med Indones 2013;45:141-7. |
| 11. | Jubiz W, Ramirez M. Effect of vitamin C on the absorption of levothyroxine in patients with hypothyroidism and gastritis. J Clin Endocrinol Metab 2014;99:E1031-4. |
| 12. | Huang Z, Liu Y, Qi G, Brand D, Zheng SG. Role of vitamin A in the immune system. J Clin Med 2018;7:258. |
| 13. | Shimizu H, Tsubota T, Kanki K, Shiota G. All-trans retinoic acid ameliorates hepatic stellate cell activation via suppression of thioredoxin interacting protein expression. J Cell Physiol 2018;233:607-16. |
| 14. | Malivindi R, Rago V, De Rose D, Gervasi MC, Cione E, Russo G, et al. Influence of all-trans retinoic acid on sperm metabolism and oxidative stress: Its involvement in the physiopathology of varicocele-associated male infertility. J Cell Physiol 2018;233:9526-37. |
| 15. | Kawaguchi R, Zhong M, Kassai M, Ter-Stepanian M, Sun H. Vitamin A transport mechanism of the multitransmembrane cell-surface receptor STRA6. Membranes (Basel) 2015;5:425-53. |
| 16. | Zimmermann MB, Wegmüller R, Zeder C, Chaouki N, Torresani T. The effects of vitamin A deficiency and vitamin A supplementation on thyroid function in goitrous children. J Clin Endocrinol Metab 2004;89:5441-7. |
| 17. | Farhangi MA, Keshavarz SA, Eshraghian M, Ostadrahimi A, Saboor-Yaraghi AA. The effect of vitamin A supplementation on thyroid function in premenopausal women. J Am Coll Nutr 2012;31:268-74. |
| 18. | Ma B, Yang P, Gao J, Du L, Sheng C, Usman T, et al. Relationship of vitamin A and thyroid function in individuals with obesity and after laparoscopic sleeve gastrectomy. Front Nutr 2022;9:824193. |
| 19. | Saleh SR, Zaki R, Hassan R, El-Kersh MA, El-Sayed MM, Abd Elmoneam AA. The impact of vitamin A supplementation on thyroid function and insulin sensitivity: Implication of deiodinases and phosphoenolpyruvate carboxykinase in male wistar rats. Eur J Nutr 2022;61:4091-105. |
| 20. | Dixon CJ, Knight T, Binns E, Ihaka B, O'Brien D. Clinical measures of balance in people with type two diabetes: A systematic literature review. Gait Posture 2017;58:325-32. |
| 21. | Padayatty SJ, Katz A, Wang Y, Eck P, Kwon O, Lee JH, et al. Vitamin C as an antioxidant: Evaluation of its role in disease prevention. J Am Coll Nutr 2003;22:18-35. |
| 22. | Tamari Y, Nawata H, Inoue E, Yoshimura A, Yoshii H, Kashino G, et al. Protective roles of ascorbic acid in oxidative stress induced by depletion of superoxide dismutase in vertebrate cells. Free Radic Res 2013;47:1-7. |
| 23. | Gillani SW, Sulaiman SA, Abdul MI, Baig MR. Combined effect of metformin with ascorbic acid versus acetyl salicylic acid on diabetes-related cardiovascular complication; A 12-month single blind multicenter randomized control trial. Cardiovasc Diabetol 2017;16:103. |
| 24. | Ashor AW, Werner AD, Lara J, Willis ND, Mathers JC, Siervo M. Effects of vitamin C supplementation on glycaemic control: A systematic review and meta-analysis of randomised controlled trials. Eur J Clin Nutr 2017;71:1371-80. |
| 25. | Zhang Y, Li R, Li Y, Chen W, Zhao S, Chen G. Vitamin A status affects obesity development and hepatic expression of key genes for fuel metabolism in zucker fatty rats. Biochem Cell Biol 2012;90:548-57. |
| 26. | Zhao S, Li R, Li Y, Chen W, Zhang Y, Chen G. Roles of vitamin A status and retinoids in glucose and fatty acid metabolism. Biochem Cell Biol 2012;90:142-52. |
| 27. | Raja Gopal Reddy M, Mullapudi Venkata S, Putcha UK, Jeyakumar SM. Vitamin A deficiency induces endoplasmic reticulum stress and apoptosis in pancreatic islet cells: Implications of stearoyl-CoA desaturase 1-mediated oleic acid synthesis. Exp Cell Res 2018;364:104-12. |
| 28. | Chien CY, Lee HS, Cho CH, Lin KI, Tosh D, Wu RR, et al. Maternal vitamin A deficiency during pregnancy affects vascularized islet development. J Nutr Biochem 2016;36:51-9. |
| 29. | Matthews KA, Rhoten WB, Driscoll HK, Chertow BS. Vitamin A deficiency impairs fetal islet development and causes subsequent glucose intolerance in adult rats. J Nutr 2004;134:1958-63. |
| 30. | Iqbal S, Naseem I. Role of vitamin A in type 2 diabetes mellitus biology: Effects of intervention therapy in a deficient state. Nutrition 2015;31:901-7. |
| 31. | Kim M, Jee SH, Kim M, Yoo HJ, Kang M, Kim J, et al. Serum vitamin A-related metabolite levels are associated with incidence of type 2 diabetes. Diabetes Metab 2017;43:287-91. |
|
Search Pubmed for