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CTRI Number  CTRI/2021/03/032373 [Registered on: 30/03/2021] Trial Registered Prospectively
Last Modified On: 18/03/2021
Post Graduate Thesis  Yes 
Type of Trial  Interventional 
Type of Study   Nutraceutical 
Study Design  Randomized, Parallel Group, Multiple Arm Trial 
Public Title of Study   Study the effect of vitamin D3 and vitamin C on glycemic control and oxidative stress markers in Type-2 Diabetes mellitus patients. 
Scientific Title of Study   A prospective, open label, 3 arm, parallel group comparative study to evaluate the effect of short term treatment with vitamin D₃ and vitamin C on glycemic control and oxidative stress markers in inadequately controlled type-2 diabetes mellitus. 
Trial Acronym   
Secondary IDs if Any  
Secondary ID  Identifier 
NIL  NIL 
 
Details of Principal Investigator or overall Trial Coordinator (multi-center study)  
Name  Shingare Sujata Prakash 
Designation  Post graduate student 
Affiliation  BYRAMJEE JEEJEEBHOY GOVERNMENT MEDICAL COLLEGE AND SASSOON GENERAL HOSPITALS, PUNE 
Address  Department of Pharmacology B.J. Govt. Medical college Jai Prakash Narayan Road, Railway Station Rd, near Pune, Maharashtra 411001

Pune
MAHARASHTRA
411001
India 
Phone  8600833063  
Fax    
Email  shingaresujata@gmail.com  
 
Details of Contact Person
Scientific Query  
Name  Dr Sujeet Anant Divhare 
Designation  Associate Professor 
Affiliation  BYRAMJEE JEEJEEBHOY GOVERNMENT MEDICAL COLLEGE AND SASSOON GENERAL HOSPITALS, PUNE 
Address  Department of Pharmacology B.J. Govt. Medical college Jai Prakash Narayan Road, Railway Station Rd, near Pune, Maharashtra 411001

Pune
MAHARASHTRA
411001
India 
Phone  9822845948  
Fax    
Email  drsujeet22@gmail.com  
 
Details of Contact Person
Public Query  
Name  Shingare Sujata Prakash 
Designation  Post graduate student 
Affiliation  BYRAMJEE JEEJEEBHOY GOVERNMENT MEDICAL COLLEGE AND SASSOON GENERAL HOSPITALS, PUNE 
Address  Department of Pharmacology B.J. Govt. Medical college Jai Prakash Narayan Road, Railway Station Rd, near Pune, Maharashtra 411001

Pune
MAHARASHTRA
411001
India 
Phone  8600833063  
Fax    
Email  shingaresujata@gmail.com  
 
Source of Monetary or Material Support  
BYRAMJEE JEEJEEBHOY GOVERNMENT MEDICAL COLLEGE AND SASSOON GENERAL HOSPITALS, Jai Prakash Narayan Road, Railway Station Rd, near Pune, Maharashtra 411001  
 
Primary Sponsor  
Name  Shingare Sujata Prakash 
Address  Department of pharmacology,BYRAMJEE JEEJEEBHOY GOVERNMENT MEDICAL COLLEGE AND SASSOON GENERAL HOSPITALS, Jai Prakash Narayan Road, Railway Station Rd, near Pune, Maharashtra 411001  
Type of Sponsor  Other [] 
 
Details of Secondary Sponsor  
Name  Address 
NIL  NIL 
 
Countries of Recruitment     India  
Sites of Study  
No of Sites = 1  
Name of Principal Investigator  Name of Site  Site Address  Phone/Fax/Email 
SHINGARE SUJATA PRAKASH  BJGMC and Sassoon hospital  MEDICINE OPD NO 60 GROUND FLOOR, PUNE
Pune
MAHARASHTRA 		 8600833063

shingaresujata@gmail.com 
 
Details of Ethics Committee  
No of Ethics Committees= 1  
Name of Committee  Approval Status 
Institutional Ethics Committee, B.J. Govt. Medical college, Sassoon General Hospital, Pune  Approved 
 
Regulatory Clearance Status from DCGI  
Status 
Not Applicable 
 
Health Condition / Problems Studied  
Health Type  Condition 
Patients  (1) ICD-10 Condition: E119||Type 2 diabetes mellitus without complications,  
 
Intervention / Comparator Agent  
Type  Name  Details 
Comparator Agent  Control group  ARM C will be Control arm and will not receive any interventional medications apart from their regular line of management. 
Intervention  Vitamin C  ARM B will receive Oral vitamin C 500mg once a day for 90 days 
Intervention  Vitamin D3  ARM A will receive Oral vitamin D3 60000IU per week for 90 days 
 
Inclusion Criteria  
Age From  30.00 Year(s)
Age To  75.00 Year(s)
Gender  Both 
Details  1. Male and female patients between 30-75yrs of age, diagnosed with
type-2 diabetes mellitus within last 1 year of collection of data.
2. Receiving oral anti-diabetic medications but does not need insulin
within last 1 year i.e. from the date of diagnosis of type-2 diabetes
mellitus.
3. Patients with HbA1c value more >7% and <9% despite therapy.
 
 
ExclusionCriteria 
Details  1. DM other than T2DM.
2. Patients with abnormal liver function tests.
3. Patients with abnormal renal function tests.
4. Patients with cardiovascular or respiratory insufficiency.
5. Acutely ill patients.
6. Pregnant and nursing women.  
 
Method of Generating Random Sequence   Computer generated randomization 
Method of Concealment   Not Applicable 
Blinding/Masking   Open Label 
Primary Outcome  
Outcome  TimePoints 
The primary outcome of this study will be reduction in HbA₁c,
which is the primary measure of glycaemic control. 		 reduction in HbA₁c during the period from day 0 to day 90
 
 
Secondary Outcome  
Outcome  TimePoints 
The secondary outcomes will be decrease in oxidative stress
and thereby decrease in the development of complications in
patients with T2DM. 		 Reduction in oxidative stress markers during the period from day 0 to day 90 
 
Target Sample Size   Total Sample Size="96"
Sample Size from India="96" 
Final Enrollment numbers achieved (Total)= "Applicable only for Completed/Terminated trials"
Final Enrollment numbers achieved (India)="Applicable only for Completed/Terminated trials" 
Phase of Trial   Phase 4 
Date of First Enrollment (India)   01/04/2021 
Date of Study Completion (India) Applicable only for Completed/Terminated trials 
Date of First Enrollment (Global)  Date Missing 
Date of Study Completion (Global) Applicable only for Completed/Terminated trials 
Estimated Duration of Trial   Years="0"
Months="9"
Days="0" 
Recruitment Status of Trial (Global)   Not Applicable 
Recruitment Status of Trial (India)  Not Yet Recruiting 
Publication Details   NIL 
Individual Participant Data (IPD) Sharing Statement

Will individual participant data (IPD) be shared publicly (including data dictionaries)?  

Response - NO
Brief Summary   Diabetes mellitus (DM) refers to a group of common metabolic disorders that share the phenotype of hyperglycemia. Several distinct types of DM are caused by a complex interaction of genetics and environmental factors. Depending on the etiology of the DM, factors contributing to hyperglycemia include reduced insulin secretion, decreased glucose utilization, and increased glucose production. The metabolic dysregulation associated with DM causes secondary pathophysiologic changes in multiple organ systems that impose a tremendous burden on the individual with diabetes and on the health care system.¹ Type 2 diabetes mellitus (T2DM) is a complex disorder influenced by both genetic and environmental factors. It is characterized by chronic hyperglycemia, altered insulin secretion, and insulin resistance.² As in many western countries, T2DM is associated with increased morbidity and mortality due to microvascular (e.g. Retinopathy, Neuropathy and Nephropathy) and macrovascular (Myocardial infarction, Peripheral vascular disease, Stroke ) complications.² Current evidence has demonstrated that oxidative stress plays an important role in the pathogenesis of chronic diseases such as DM and may diminish the antioxidative defense system of the body, increasing the oxidative load.³ The damaging effects of oxidative stress are mainly caused by the production of free radicals of oxygen and reactive oxygen species (ROS).³ It is believed that diabetes is associated with increased oxidative stress because of increased blood concentrations of thiobarbituric acid reactive substances and serum malondialdehyde, the end products of lipid peroxidation.³ Lowering glycated heamoglobin (HbA₁c) to below 7% has been shown one of the primary endpoints in reducing microvascular complications of diabetes mellitus and possibly macrovascular disease.³⁻⁴ Although therapies for T2DM and its co-morbidity have improved over the last few decades, the need for new insights for the prevention and management of T2DM remains needed due to the increased impact of the disease.⁵ There is accumulating evidence suggesting that vitamin D status plays a role in many non-skeletal functions including diabetes mellitus.⁵ Vitamin D deficiency appears to be related to the development of diabetes mellitus type 2.⁶ Renewed interest in vitamin D, the so-called “sunshine vitamin,” has occurred recently because it has been linked to everything from cancer and heart disease to diabetes.⁷ There is growing evidence that vitamin D deficiency could be a contributing factor in the development of both type 1 and type2 diabetes. First, the β-cell in the pancreas that secretes insulin has been shown to contain VDRs as well as the 1 alpha hydroxylase enzyme.⁷ Vitamin D was found to be involved in maintenance of glucose homeostasis through numerous mechanisms connected with the insulin signaling pathway. Vitamin D takes part in sustaining of normal level of Ca2+ and reactive oxygen species (ROS) both in pancreatic beta cells and insulin responsive cells.⁸ Vitamin D is required for and improves the production of insulin, and also improves insulin sensitivity.⁹ D3 can be combined with Vitamin D3 receptor on the islet β cells, increasing insulin sensitivity, inhibiting inflammatory factors, alleviating chronic inflammation process of the pancreas to improve the function of islet β cells ; Additionally, it also inhibits the action of the renin-angiotensin system, which promotes insulin secretion . Vitamin D supplementation can improve islet β cell function and glucose tolerance.¹⁰ It regulates adipogenesis during adipocyte differentiation, stimulates insulin synthesis, protects pancreatic B cells and decreases insulin resistance in muscles.¹¹ Studies have shown that vitamin D deficiency is associated with the development of T2D, T2D nephropathy, T2D microvascular or macrovascular disease, diabetic retinopathy, and diabetic peripheral neuropathy.¹²⁻¹³ In addition, diabetes mellitus (DM) and chronic kidney disease (CKD) are also related to vitamin D levels, vitamin D influences the renin-angiotensin system, inflammation, and mineral bone disease, which may be associated with the cause and progression CKD.¹⁴ It has been revealed that vitamin D plays an important role in reducing inflammation and controlling immune activation.¹⁵ Oxidative stress plays a central role in the onset of diabetes mellitus as well as in the development of vascular and neurological complications of the disease. ¹⁶ Consumption of antioxidants nutrients, chiefly vitamin C and E seems to decrease oxidative injury associated with hyperglycemia and pancreatic β cell function and reduces the prevalence of diabetic complications.¹⁶ ROS are involved both in insulin signal transduction and in insulin resistance when produced in excess.¹⁶ Vitamin C, also known as ascorbic acid, is a cofactor in multiple enzymatic reactions including collagen synthesis. Vitamin C acts as a reducing agent in free radical-mediated oxidation processes; therefore, it can act as an antioxidant.¹⁷ Vitamin C is structurally similar to glucose and can replace it in many chemical reactions and thus is effective for prevention of non-enzymatic glycosylation of protein.¹⁸ Ascorbic acid (vitamin C), an antioxidant vitamin, plays an important role in protecting free radical-induced damage.¹⁸ Antioxidant treatment has beneficial effects on preservation of β cell function in diabetes.¹⁸ Diabetes mellitus is a major health problem with serious and severe complications, therefore, in order to improve management and outcome, we have designed this study to evaluate if the administration of vitamin D and vitamin C improves glycemic control as well as reduces complications.  
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