Pyridoxal-5-phosphate (P.L.P.), the biologically active form of vitamin B6, is a coenzyme in 150 enzymatic reactions, including amino acid, carbohydrate, and lipid metabolism. Neurotransmitter production and breakdown depend on it. Additionally, it functions as an antioxidant by suppressing reactive oxygen species and mitigating the development of advanced glycation end products. Humans recycle P.L.P. from dietary B6 vitamins, and this molecule has been related to various clinically relevant diseases. Pyridoxine as an additional therapy for type 2 diabetes will be examined in this study.

Numerous organs might suffer long-term harm, malfunction, and failure as a result of type 2 diabetes. While the illness may initially cause weight loss, frequent urination, thirst, and hazy vision, the long-term repercussions may include the gradual onset of specific issues such as cardiovascular disease (CVD), retinopathy, which may culminate in blindness, and renal disease. The risk of foot ulcers, Charcot joints, and symptoms of autonomic dysfunction, such as sexual dysfunction, is associated with renal failure and/or neuropathy. Diabetes and vitamin B6 have both been linked. It is not apparent, therefore, whether diabetes is a consequence of low P.L.P. levels, a cause, or both. According to some study, diabetes may develop as a consequence of low P.L.P. levels, however other studies suggest that diabetes decreases P.L.P. levels. Although the physiological and molecular pathways behind these beneficial effects on diabetic pathology and related repercussions are not completely understood, multiple investigations have demonstrated that B6 therapy has good effects. There are numerous ways that pyridoxal 5-phosphate deficiency affects diabetes. As an essential element for numerous enzymes that contribute to this process, pyridoxal-5-phosphate can, for example, influence the route that converts tryptophan into niacin. It has been proven that the metabolites produced when this pathway is damaged lessen the bioactivity of insulin and cause insulin resistance, a T2D symptom . Pyridoxal-5-phosphate may influence insulin resistance via modulating the expression of adipogenesis-related genes. The degradation of co-enzyme-dependent enzymes like (C.B.S.) and (C.G.L.), which rely on pyridoxal-5-phosphate, may also promote insulin resistance via elevating homocysteine levels .

This research intends to examine the impact of pyridoxine adjuvant treatment on the blood glucose level in type 2 diabetes patients.

This is a randomized controlled open-label interventional study. T2DM patients who receive either (metformin with pyridoxine) or (metformin only) daily and T2DM patients treated with non-pharmacological therapy (lifestyle modification) will be included in the study.

Inclusion Criteria:

• Type 2 Diabetes mellitus newly diagnosed patient with age (Above 30) years.
• HbA1c less than or equal to 7.5%.

Exclusion Criteria:

• Type 1 Diabetes mellitus.
• Concomitant chronic diseases (Rheumatoid arthritis, anemia, asthma, endocrine disorders, renal failure, alcoholics, and patient on anti-T.B. or anti-epileptics).
• Females should be neither pregnant nor on oral contraceptive drugs.
• Not taking any vitamin or mineral supplementation.
• Should have no history of recent acute infection (within the previous two weeks).