An interventional study of Experimental group: Exercise training in Type 2 Diabetes, Lifestyle-related Condition and Insulin Sensitivity/Resistance, sponsored by Finis Terrae University. Recruiting at 1 site in Chile. Open to participants aged 45 Years to 75 Years. Per ClinicalTrials.gov, last updated 2026-03-16.
Sponsored by Finis Terrae University · Not applicable, Interventional, and Treatment
A recognized driver for cardiovascular complications of type 2 diabetes mellitus (T2DM) is impaired plasma glucose homeostasis as consequence of skeletal muscle insulin resistance. Insulin-mediated plasma glucose disposal in skeletal muscle comprises oxidative glucose disposal (cellular glucose uptake for oxidation) and non-oxidative glucose disposal (NOGD; cellular glucose uptake for storage as glycogen), both processes being impaired in T2DM patients. Excessive intrahepatic fat accumulation (particularly monounsaturated (MUFA) and saturated (SFA)) is commonly observed in T2DM patients and tightly associates with plasma glucose dysregulation. It has been hypothesized that skeletal muscle insulin resistance redistributes circulating glucose away from muscle which together with hyperinsulinemia promotes intrahepatic lipid accretion via de novo lipogenesis (DNL). As saturated lipids is the final product of DNL, improving skeletal muscle insulin sensitivity, next to enhance plasma glucose homeostasis, might lower intrahepatic lipid content particularly intrahepatic saturated lipids.
Regular exercise is a cornerstone in the treatment of T2DM and to improve skeletal muscle insulin sensitivity. Interestingly, a conventional exercise program (aerobic-type combined with strength-type exercise) restores insulin-stimulated oxidative glucose disposal in T2DM patients to levels observed in age-matched normoglycemic subjects. Non-oxidative glucose disposal (NOGD), however, does not improve upon such conventional exercise programs. In this regard, for full restoration of compromised glucose disposal, it is pivotal to come up with effective training methods to target NOGD. High intensity interval training (HIIT) has the potential to expands the glycogen synthesis capacity in athletes by repetitive cycles of glycogen depletion/repletion, hence holds promise to improve NOGD in T2DM patients. Of note, HIIT also lowers the intrahepatic fat content in pre-diabetes individuals. Nevertheless, whether HIIT reduces the intrahepatic fat content and modifies its composition in T2DM patients is unknown. In this regard, it is hypothesized that HIIT expands the NOGD capacity in skeletal muscle of overweight/obese type 2 diabetes patients. By doing so, it is postulated that HIIT improves skeletal muscle insulin sensitivity and therefore benefits the 24 hours glycaemic profile in T2DM patients. In line, it is hypothesized that the HIIT-mediated improvements on NOGD and skeletal muscle insulin sensitivity coexist with the reduction of intrahepatic lipid content -particularly reduced saturated lipids- via lowering DNL.
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Exclusion Criteria:
This arm will perform HIIT under supervision. The post training condition of this arm will be compared to an age and BMI matched, normoglycemic non-intervention group.
Other: Experimental group: Exercise training
This corresponds to a non-training, control group, of age-, BMI matched, type 2 diabetes individuals.
A group of normoglycemic individuals will the reference comparison for the T2D-HIIT arm post-intervention
HIIT program, 3 times per week for 12 weeks
Insulin-stimulated non-oxidative plasma glucose disposal (NOGD)
Insulin-stimulated NOGD will be measured upon hyperinsulinemic-euglycemic clamp test
Time frame: 12 weeks
Skeletal muscle insulin sensitivity
Skeletal muscle insulin sensitivity will be measured as the rate of insulin-stimulated plasma glucose disposal (Rd) measured upon hyperinsulinemic-euglycemic clamp test
Time frame: 12 weeks
Insulin-stimulated glucose oxidation
Insulin-stimulated glucose oxidation will be measured via indirect calorimetry during clamp test
Time frame: 12 weeks
Metabolic flexibility
Metabolic flexibility will be measured via indirect calorimetry during the clamp test
Time frame: 12 weeks
Liver insulin sensitivity
Liver insulin sensitivity will be measured as the rate of insulin-mediated suppression of endogenous glucose production (EGP) upon hyperinsulinemic-euglycemic clamp test
Time frame: 12 weeks
24 hours glycemic profile
24 hours glycemic profile will be measured by the use of continuous glucose monitoring device
Time frame: 12 weeks
Intrahepatic lipid content and composition
Intrahepatic lipid content and composition will be measured by magnetic resonance spectroscopy of protons (1H-MRS)
Time frame: 12 weeks
De novo lipogenesis (DNL)
DNL will be measured by the use of deuterated water (D2O)
Time frame: 12 weeks
Skeletal muscle glycogen content
Muscle glycogen content will be quantified in muscle biopsies
Time frame: 12 weeks
Proteins that regulate oxidative metabolism
Content of proteins that regulate oxidative phosphorylation system (OXPHOS) will be quantified in muscle biopsies
Time frame: 12 weeks
Maximal aerobic capacity
Maximal aerobic capacity will be measure upon a progressive cycling test
Time frame: 12 weeks
Body weight
Body weight will be measured in kilograms
Time frame: 12 weeks
Total muscle mass
total muscle mass will be measured in kilograms and/or percentage
Time frame: 12 weeks
Total fat mass
Total fat mass will be measured in kilograms and/or percentage
Time frame: 12 weeks
Fat-free mass
Fat-free mass will be measured in kilograms and/or percentage
Time frame: 12 weeks
Skeletal muscle mutiomics
multiomics will be applied in muscle biopsies
Time frame: 12 weeks
Plan to share: No
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Finis Terrae University