The Effect of Exercise on Hepatic Glucose Metabolism

This study is enrolling participants by invitation only.
Sponsor:
Information provided by (Responsible Party):
Jason Winnick, Vanderbilt University
ClinicalTrials.gov Identifier:
NCT01783275
First received: July 19, 2012
Last updated: January 31, 2013
Last verified: January 2013

July 19, 2012
January 31, 2013
February 2013
September 2015   (final data collection date for primary outcome measure)
Splanchnic glucose uptake [ Time Frame: 3 years ] [ Designated as safety issue: No ]
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.
Same as current
Complete list of historical versions of study NCT01783275 on ClinicalTrials.gov Archive Site
Endogenous glucose production [ Time Frame: 3 years ] [ Designated as safety issue: No ]
Increases in hepatic insulin sensitivity as a result of lifestyle intervention will cause reduced EGP during the fasted state, and in response to hyperinsulinemia. This reduction will be accounted for by reductions in glycogenolysis
Same as current
Not Provided
Not Provided
 
The Effect of Exercise on Hepatic Glucose Metabolism
The Effect of Exercise on Hepatic Glucose Metabolism in Type 2 Diabetes Mellitus

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 either exercise training or weight loss, will increase the amount of glucose from an oral load that is taken up by the liver in subjects with DM. We also hypothesize that the amount of glucose taken up by the liver will be increased even further in response to exercise training plus weight loss compared to either treatment alone.

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

Not Provided
Interventional
Not Provided
Allocation: Non-Randomized
Intervention Model: Parallel Assignment
Masking: Open Label
  • Obesity
  • Type 2 Diabetes
  • Behavioral: Aerobic exercise
    12 weeks of aerobic exercise with weight maintenance
  • Behavioral: Weight loss
    12 weeks of caloric restriction to achieve 7-10% weight loss
  • Experimental: Aerobic Exercise
    12 weeks of aerobic exercise
    Intervention: Behavioral: Aerobic exercise
  • Experimental: Weight Loss
    12 weeks of low calorie diet to achieve 7-10% weight loss
    Intervention: Behavioral: Weight loss
  • Experimental: Aerobic Exercise with weight loss
    12 weeks of aerobic exercise with reduced caloric intake to achieve 7 - 10% weight loss
    Interventions:
    • Behavioral: Aerobic exercise
    • Behavioral: Weight loss
  • No Intervention: Control
    12 weeks with no change in diet or exercise habits (weight maintenance).
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Enrolling by invitation
68
September 2015
September 2015   (final data collection date for primary outcome measure)

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
Both
40 Years to 60 Years
No
Contact information is only displayed when the study is recruiting subjects
United States
 
NCT01783275
121031, DK093799
No
Jason Winnick, Vanderbilt University
Vanderbilt University
Not Provided
Principal Investigator: Jason Winnick, PhD Vanderbilt University
Study Chair: Naji Abumrad, MD Vanderbilt University
Vanderbilt University
January 2013

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP