The Reduction in Glucose Stimulated Insulin Secretion Induced by Cytokines May be Prevented by Copper Addition - Studies in Diabetic Patients

NCT00846144 | Unknown

• 1 other identifier: 0136-08-HMO
• Study Type: interventional
• Target: 100
• Locations: 1 country
• Sites: 1

Brief Summary

In the CDs rat model, beta-cell dysfunction and pancreatic exocrine damage are triggered and prevented by altering dietary Cu content suggesting a chronic and acute role for Cu. These abnormalities become apparent when the CDs rats are exposed to high sucrose low copper diet, triggering a vicious sequence of events: exocrine damage, recruitment of macrophages expressing IL-1beta leading to oxidative stress and even more reduction in the activity of Cu-dependent enzymes (chronic effect). When Cu levels are re-established (acute effect) they may prevent the inhibitory effect of IL-1beta on insulin release and may restore the activity of enzymes inhibited by IL-1beta. In this study we will identify humans with marginal Cu status that may benefit from copper supplementation to normalize their GSIS. These patients will be given a daily Cu supplement (3mg/d), or placebo for a period of 6 months. GSIS, pancreatic dysfunction and biomarkers of marginal Cu status will be measured in different blood components before and every 4 weeks during treatments or placebo.

Conditions

Hyperglycemia; Diabetes

Keywords

Glucose stimulated insulin secretion; copper; cytokines; diabetes; Reduction in insulin secretion

Outcome Measures

Primary Outcomes (1)

• Identify humans with marginal Cu status that may benefit from copper supplementation and normalize their GSIS.

  6 months

Interventions

copper sulfate DIETARY_SUPPLEMENT

copper sulfate 3mg/d for a period of 6 months

Eligibility Criteria

• Age: 30 Years - 80 Years
• Sex: all
• Healthy Volunteers: Yes
• Age Groups: Adult (18-64), Older Adult (65+)

You may qualify if:

• diabetic subjects with BMI \< 33
• HbA1C \< 8
• plasma copper levels of \< 90 ul/dl

You may not qualify if:

• patients with bad physical conditions

Sponsors & Collaborators

• Hadassah Medical Organization: lead

Study Sites (1)

Diabetes Unit, Hadassah Medical Organization

Jerusalem, 91120, Israel

Location

Related Publications (2)

• Weksler-Zangen S, Raz I, Lenzen S, Jorns A, Ehrenfeld S, Amir G, Oprescu A, Yagil Y, Yagil C, Zangen DH, Kaiser N. Impaired glucose-stimulated insulin secretion is coupled with exocrine pancreatic lesions in the Cohen diabetic rat. Diabetes. 2008 Feb;57(2):279-87. doi: 10.2337/db07-0520. Epub 2007 Oct 31.

  PMID: 17977959 BACKGROUND

• Weksler-Zangen S, Yagil C, Zangen DH, Ornoy A, Jacob HJ, Yagil Y. The newly inbred cohen diabetic rat: a nonobese normolipidemic genetic model of diet-induced type 2 diabetes expressing sex differences. Diabetes. 2001 Nov;50(11):2521-9. doi: 10.2337/diabetes.50.11.2521.

  PMID: 11679430 BACKGROUND

MeSH Terms

Conditions

Hyperglycemia; Diabetes Mellitus

Interventions

Copper Sulfate

Condition Hierarchy (Ancestors)

Glucose Metabolism Disorders; Metabolic Diseases; Nutritional and Metabolic Diseases; Endocrine System Diseases

Intervention Hierarchy (Ancestors)

Sulfates; Sulfuric Acids; Sulfur Acids; Sulfur Compounds; Inorganic Chemicals

Study Officials

• Itamar Raz, Prof

  Hadassah Medical Organization

  PRINCIPAL INVESTIGATOR

Central Study Contacts

Itamar Raz, Prof

CONTACT

972-2-6778021; ntv502@netvision.net.il

Study Design

• Study Type: interventional
• Phase: not applicable
• Allocation: NA
• Masking: NONE
• Purpose: PREVENTION
• Intervention Model: SINGLE GROUP
• Sponsor Type: OTHER

Study Record Dates

• First Submitted: February 17, 2009
• First Posted: February 18, 2009
• Study Start: September 1, 2009
• Primary Completion: September 1, 2010
• Study Completion: December 1, 2010
• Last Updated: February 18, 2009

Record last verified: 2009-02

Locations

IL (1)