Ignite Creation Date:
2025-12-24 @ 5:31 PM
Ignite Modification Date:
2025-12-30 @ 7:53 AM
Study NCT ID:
NCT05902468
Status:
UNKNOWN
Last Update Posted:
2023-06-15
First Post:
2023-06-05
Is NOT Gene Therapy:
True
Has Adverse Events:
False
Brief Title:
Ursodeoxycholic Acid as add-on Therapy in Type 2 Diabetes Mellitus
Sponsor:
Tanta University
Organization:
Study Overview
Official Title:
A Clinical Study Evaluating the Use od Ursodeoxycholic Acid as Adjuvant Therapy in Type 2 Diabetes Mellitus
Status:
UNKNOWN
Status Verified Date:
2023-06
Last Known Status:
RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Diabetes mellitus (DM) is a complex metabolic disorder characterized by hyperglycemia and abnormalities in carbohydrate, fat, and protein metabolism. It is one of the most prevalent metabolic disorders globally. Despite the advancement in anti-diabetic drug therapy, most patients fail to achieve optimal glycemic control. therefore, there is a large unmet need to develop new strategies to improve the therapeutic outcomes in diabetic patients. This study is designed to evaluate the efficacy of ursodeoxycholic acid as adjunctive therapy in patients with type 2 diabetes mellitus.
Detailed Description:
Diabetes mellitus (DM) is a complex metabolic disorder characterized by hyperglycemia and abnormalities in carbohydrate, fat, and protein metabolism. It is one of the most prevalent metabolic disorders globally. More than 75% of diabetic patients live in low- and middle-income countries. About 90% of diabetic patients have type 2 diabetes.
Insulin resistance (IR) and β-cell dysfunction are the two main pathophysiological events contributing to type 2 diabetes.
Insulin resistance is a pathological condition in which insulin-dependent tissues fail to properly respond to normal circulatory levels of insulin. Inflammatory mediators play a key role in insulin resistance. For example, tumor necrosis factor alpha (TNF-α) impairs insulin signaling via serine phosphorylation of insulin receptor substrate (IRS-1). Additionally, it reduces glucose transporter-4 (GLUT-4) expression, limiting glucose entry into adipocytes and skeletal muscle cells. Similarly, IL-6 induces IRS degradation. Oxidative stress interferes with insulin signal transduction leading to IR. It activates several serine-threonine kinase pathways, which, in turn, phosphorylates IRS proteins leading to subsequent degradation.
β-cell dysfunction is associated with β-cell death. In an excessive nutritional state, as in obesity, hyperglycemia and hyperlipidemia are often present, favoring IR and chronic inflammation. Under these circumstances, β-cells are subject to toxic pressures including inflammation, endoplasmic reticulum stress, oxidative stress, as well as amyloid stress, that ultimately lead to loss of islet integrity.
Ursodeoxycholic acid (UDCA) is an endogenous hydrophilic bile acid normally present in human bile and traditionally used for the treatment of liver diseases. UDCA has direct antioxidant properties. It decreased glucose levels, alleviated hyperinsulinemia, and improved islet function in rats with liver fibrosis. Therefore, this study is designed to evaluate the efficacy of ursodeoxycholic acid as adjunctive therapy in patients with type 2 diabetes mellitus.
Insulin resistance (IR) and β-cell dysfunction are the two main pathophysiological events contributing to type 2 diabetes.
Insulin resistance is a pathological condition in which insulin-dependent tissues fail to properly respond to normal circulatory levels of insulin. Inflammatory mediators play a key role in insulin resistance. For example, tumor necrosis factor alpha (TNF-α) impairs insulin signaling via serine phosphorylation of insulin receptor substrate (IRS-1). Additionally, it reduces glucose transporter-4 (GLUT-4) expression, limiting glucose entry into adipocytes and skeletal muscle cells. Similarly, IL-6 induces IRS degradation. Oxidative stress interferes with insulin signal transduction leading to IR. It activates several serine-threonine kinase pathways, which, in turn, phosphorylates IRS proteins leading to subsequent degradation.
β-cell dysfunction is associated with β-cell death. In an excessive nutritional state, as in obesity, hyperglycemia and hyperlipidemia are often present, favoring IR and chronic inflammation. Under these circumstances, β-cells are subject to toxic pressures including inflammation, endoplasmic reticulum stress, oxidative stress, as well as amyloid stress, that ultimately lead to loss of islet integrity.
Ursodeoxycholic acid (UDCA) is an endogenous hydrophilic bile acid normally present in human bile and traditionally used for the treatment of liver diseases. UDCA has direct antioxidant properties. It decreased glucose levels, alleviated hyperinsulinemia, and improved islet function in rats with liver fibrosis. Therefore, this study is designed to evaluate the efficacy of ursodeoxycholic acid as adjunctive therapy in patients with type 2 diabetes mellitus.
Study Oversight
Has Oversight DMC:
True
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?: