The Effect of Exercise on Hepatic Glucose Metabolism

Obesity Clinical Trial

Official title:

The Effect of Exercise on Hepatic Glucose Metabolism in Type 2 Diabetes Mellitus

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT01783275
• Other study ID #: 121031
• Secondary ID: DK093799
• Status: Completed
• Phase: N/A
• Start date: February 2013
• Est. completion date: September 2016

Study information

• Verified date: August 2018
• Source: Vanderbilt University Medical Center
• Contact: n/a
• Is FDA regulated: No
• Study type: Interventional

Clinical Trial Summary

It is known that obesity and/or physical inactivity greatly increase a person's risk of developing heart disease and other serious health problems. This is partly because diabetes is associated with inflammation, oxidative stress, and insulin resistance. Diabetes is also associated with high levels of triglycerides in the blood and tissues such as the liver (known as fatty liver or steatosis). This elevation of fat in the liver is known to cause liver insulin resistance and impair the function of the liver and this impairment contributes to the development of diabetes.

Studies have shown that both aerobic exercise and weight loss have beneficial results on insulin resistance. However, the cause of this benefit remains unclear. We know that both aerobic exercise and/or weight loss can improve how muscle responds to insulin. However, it is also known that aerobic exercise and/or weight loss lowers liver fat content, thereby making it possible that the liver's response to insulin is also improved by weight loss and/or exercise training. An improved responsiveness of the liver to insulin could lower blood sugar levels after a meal and it could also lower morning blood sugar levels. However, very little is known about how exercise and/or weight loss improves liver function in people with type 2 diabetes.

Hypothesis 1: Improved hepatic insulin sensitivity, as a result of exercise training will increase the amount of glucose from an oral load that is taken up by the liver in subjects with DM.

Hypothesis 2: Increases in hepatic insulin sensitivity as a result of exercise will cause reductions in EGP during the fasted state, and will improve the suppression of EGP seen in response to hyperinsulinemia.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 20
• Est. completion date: September 2016
• Est. primary completion date: September 2016
• Accepts healthy volunteers: No
• Gender: All
• Age group: 40 Years to 60 Years

Eligibility

Inclusion Criteria:

• 40-60 yrs of age

• sedentary lifestyle

• stable weight

• BMI 30 - 40kg/m2

• Hgb A1c <8.5

• Type 2 diabetes

Exclusion Criteria:

• Use of insulin

• Use of TZDs

Related Conditions & MeSH terms

• Diabetes Mellitus, Type 2
• Obesity
• Type 2 Diabetes

Intervention

Behavioral:
• Aerobic exercise
12 weeks of aerobic exercise with weight maintenance

Locations

Country	Name	City	State
United States	Vanderbilt University Medical Center	Nashville	Tennessee

Sponsors (1)

Lead Sponsor	Collaborator
Vanderbilt University

Country where clinical trial is conducted

United States, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Splanchnic glucose uptake	Improved hepatic insulin sensitivity, as a result of lifestyle intervention, will increase the amount of glucose from an oral load that is taken up by the liver in subjects with DM.	3 years
Secondary	Endogenous glucose production	Increases in hepatic insulin sensitivity as a result of lifestyle intervention will cause reduced EGP during the fasted state, and in response to hyperinsulinemia.	3 years