Skeletal Muscles, Myokines and Glucose Metabolism MYOGLU

NCT01803568 | Completed

• 1 other identifier: 2011/882
• Study Type: interventional
• Target: 31
• Locations: 0 countries
• Sites: N/A

Brief Summary

Normal glucose uptake and metabolism in skeletal muscles are essential to keep blood glucose within normal range and hence, insulin resistance (possibly mediated by inflammatory processes) in skeletal muscle is a major pathogenic factor in type 2 diabetes. Physical activity seems to be of essential importance in the prevention and treatment of type 2 diabetes. Myokines are proteins secreted from skeletal muscle that can execute important biological functions locally in the muscle (paracrine) or in other organs like the brain, heart and pancreas (endocrine). Evidence suggest that several interleukines and other cytokines are secreted by skeletal muscles. In the present project, the investigators will explore the relation between secreted myokines from muscle cells, insulin resistance and glucose metabolism before and after 12 weeks of exercise intervention. Subjects with normal as well as impaired glucose metabolism will be included in the study.

Conditions

Hyperglycemia; Normoglycemia; Myokine

Keywords

Myokine; Insulin sensitivity; Exercise; Skeletal muscle

Outcome Measures

Primary Outcomes (2)

• Change from baseline in gene expression changes in skeletal and adipose tissue

  Baseline and after 12 weeks, and before, 0 hr and 2 hours after acute exercise

• Changes from baseline in plasma/serum levels of selected proteins

  Baseline and after 12 weeks, and before, 0 hr and 2 hour

Secondary Outcomes (5)

• Change from baseline in insulin sensitivity

  Before and after 12 weeks of exercise

• Changes in baseline from maximal oxygen uptake VO2 max

  Before and after 12 weeks

• Changes from baseline in muscle strength

  Before and after 12 weeks

• Changes from baseline in body composition

  Before and after 12 weeks

• Changes from baseline in heart frequency

  Before and after 12 weeks

Study Arms (2)

Exercise in normoglycaemic individuals

EXPERIMENTAL

Other: Exercise

Exercise in hyperglycaemic individuals

EXPERIMENTAL

Other: Exercise

Interventions

Exercise OTHER

12 weeks of exercise; 4 times pr week

Exercise in hyperglycaemic individuals; Exercise in normoglycaemic individuals

Eligibility Criteria

• Age: 40 Years - 65 Years
• Sex: male
• Healthy Volunteers: Yes
• Age Groups: Adult (18-64), Older Adult (65+)

You may qualify if:

• Male
• Age 40-65 years
• Nordic ethnicity
• Non-smoker
• Either (participants with impaired glucose metabolism): Body Mass Index (BMI) 27-32 kg/m2 and abnormal glucose metabolism, defined as:
• i. impaired fasting glucose (FPG ≥ 5.6 mmol/L) ii. impaired glucose tolerance (2 h PG ≥7.8 mmol/L) iii. type 2 diabetes (no medication, HbA1c ≤7.5%)
• Or (controls): BMI 19-25 kg/m2 and normal glucose metabolism and no first degree relatives with type 2 diabetes.

You may not qualify if:

• Subjects having type 1 diabetes or medically treated type 2 diabetes.
• Systolic blood pressure ≥ 160 mmHg or diastolic blood pressure ≥ 90 mmHg at screening
• Significant hematological or renal disease or chronic renal impairment, GFR\< 50 ml/min.
• Significant liver disease or ALAT \>3x UNL.
• Chronic inflammatory disease in active phase or long-term use of corticosteroids last 3 months.
• Use of anti-diabetic agents, lipid lowering drugs, antihypertensive medication, ASA or any other drug not deemed suitable by the study physician.
• Mental condition (psychiatric or organic cerebral disease), drug or alcohol abuse rendering the subject unable to understand the nature, scope and possible consequences of the study.
• Smoker
• Any medical or other condition that in the judgment of the investigator would jeopardize the subject's safety or evaluation of the intervention for efficacy and safety
• Exercising regularly (\>1 times pr week)

Sponsors & Collaborators

• Oslo University Hospital: lead
• University of Oslo: collaborator
• Norwegian School of Sport Sciences: collaborator

Related Publications (7)

• Lee-Odegard S, Austin Argentieri M, Norheim F, Drevon CA, Birkeland KI. Reversal of proteomic aging with exercise-results from the UK biobank and a 12-week intervention study. NPJ Aging. 2025 Dec 26. doi: 10.1038/s41514-025-00318-w. Online ahead of print.

  PMID: 41449222 DERIVED

• Lee-Odegard S, Hjorth M, Olsen T, Moen GH, Daubney E, Evans DM, Hevener AL, Lusis AJ, Zhou M, Seldin MM, Allayee H, Hilser J, Viken JK, Gulseth H, Norheim F, Drevon CA, Birkeland KI. Serum proteomic profiling of physical activity reveals CD300LG as a novel exerkine with a potential causal link to glucose homeostasis. Elife. 2024 Aug 27;13:RP96535. doi: 10.7554/eLife.96535.

  PMID: 39190027 DERIVED

• Doncheva AI, Romero S, Ramirez-Garrastacho M, Lee S, Kolnes KJ, Tangen DS, Olsen T, Drevon CA, Llorente A, Dalen KT, Hjorth M. Extracellular vesicles and microRNAs are altered in response to exercise, insulin sensitivity and overweight. Acta Physiol (Oxf). 2022 Dec;236(4):e13862. doi: 10.1111/apha.13862. Epub 2022 Aug 10.

  PMID: 36377504 DERIVED

• Moore TM, Zhou Z, Cohn W, Norheim F, Lin AJ, Kalajian N, Strumwasser AR, Cory K, Whitney K, Ho T, Ho T, Lee JL, Rucker DH, Shirihai O, van der Bliek AM, Whitelegge JP, Seldin MM, Lusis AJ, Lee S, Drevon CA, Mahata SK, Turcotte LP, Hevener AL. The impact of exercise on mitochondrial dynamics and the role of Drp1 in exercise performance and training adaptations in skeletal muscle. Mol Metab. 2019 Mar;21:51-67. doi: 10.1016/j.molmet.2018.11.012. Epub 2018 Dec 4.

  PMID: 30591411 DERIVED

• Lee S, Norheim F, Gulseth HL, Langleite TM, Aker A, Gundersen TE, Holen T, Birkeland KI, Drevon CA. Skeletal muscle phosphatidylcholine and phosphatidylethanolamine respond to exercise and influence insulin sensitivity in men. Sci Rep. 2018 Apr 25;8(1):6531. doi: 10.1038/s41598-018-24976-x.

  PMID: 29695812 DERIVED

• Sommer C, Lee S, Gulseth HL, Jensen J, Drevon CA, Birkeland KI. Soluble Leptin Receptor Predicts Insulin Sensitivity and Correlates With Upregulation of Metabolic Pathways in Men. J Clin Endocrinol Metab. 2018 Mar 1;103(3):1024-1032. doi: 10.1210/jc.2017-02126.

  PMID: 29300960 DERIVED

• Lee S, Norheim F, Langleite TM, Noreng HJ, Storas TH, Afman LA, Frost G, Bell JD, Thomas EL, Kolnes KJ, Tangen DS, Stadheim HK, Gilfillan GD, Gulseth HL, Birkeland KI, Jensen J, Drevon CA, Holen T; NutriTech Consortium. Effect of energy restriction and physical exercise intervention on phenotypic flexibility as examined by transcriptomics analyses of mRNA from adipose tissue and whole body magnetic resonance imaging. Physiol Rep. 2016 Nov;4(21):e13019. doi: 10.14814/phy2.13019.

  PMID: 27821717 DERIVED

MeSH Terms

Conditions

Hyperglycemia; Insulin Resistance; Motor Activity

Interventions

Exercise

Condition Hierarchy (Ancestors)

Glucose Metabolism Disorders; Metabolic Diseases; Nutritional and Metabolic Diseases; Hyperinsulinism; Behavior

Intervention Hierarchy (Ancestors)

Motor Activity; Movement; Musculoskeletal Physiological Phenomena; Musculoskeletal and Neural Physiological Phenomena

Study Officials

• Kåre I Birkeland, MD PhD

  Oslo University Hospital

  PRINCIPAL INVESTIGATOR

• Christian A Drevon, MD PhD

  University of Oslo

  STUDY CHAIR

Study Design

• Study Type: interventional
• Phase: not applicable
• Allocation: NON RANDOMIZED
• Masking: NONE
• Purpose: BASIC SCIENCE
• Intervention Model: PARALLEL
• Sponsor Type: OTHER
• Responsible Party: PRINCIPAL INVESTIGATOR
• PI Title: Professor

Study Record Dates

• First Submitted: February 26, 2013
• First Posted: March 4, 2013
• Study Start: September 1, 2011
• Primary Completion: December 1, 2012
• Study Completion: December 1, 2012
• Last Updated: March 4, 2013

Record last verified: 2013-03