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Recruiting NCT01477957

The Effect of Bariatric Surgery on Insulin Sensitivity and Energy Metabolism

— Observational Obesity Diabetes Mellitus, Type 2

For patients and families

In plain language

An automatic summary of structured registry data. It is an orientation aid, not a substitute for the official protocol or a physician assessment.

What is being studied
The protocol lists: surgery.
Who it may be relevant to
Registry conditions: Obesity, Diabetes Mellitus, Type 2. Basic parameters: 20 years — 70 years · All.
What needs checking
Age, condition and sex are only basic indicators. Prior treatment, laboratory values and other mandatory requirements appear in the eligibility criteria below.
Where it takes place
Germany
Next step
Save the trial, show it to the treating physician, and confirm current recruitment with the study center. Costs, documents and travel →

Unsure about the terms? Read our patient guide →

Official title

The Effect of Bariatric Surgery on Insulin Sensitivity and Energy Metabolism in Obesity Grade 2 -3

Overview

The purpose of this study is: 1. To explore to what extent insulin sensitivity, energy metabolism and ectopic lipid storage can be improved by bariatric surgery 2. To explore to what extent hepatic and muscular disorders of energy metabolism occur in patients with obesity (degree 2-3) 3. To explore whether the steato liver occurring in patients with obesity (degree 2-3) is associated with the degree of liver inflammation

Detailed description

Insulin resistance strongly relates to ectopic lipid deposition in skeletal muscle and the liver, which correlate with insulin resistance. Lipid metabolites accumulating in skeletal muscle and the liver are thought to impair insulin signalling and thereby reduce glucose uptake and glycogen storage. Insulin resistant humans frequently present with decreased mitochondrial function in skeletal muscle which might contribute to lipid accumulation and the development of insulin resistance. Metabolic dysfunction-associated steatotic liver disease comprises steatosis, steatohepatitis and cirrhosis. MASLD correlates with insulin resistance, increased risk for cardiovascular diseases and type 2 diabetes. The mechanisms leading from steatosis to steatohepatitis and insulin resistance in the liver are yet unclear. Bariatric surgery aims at profound reduction of body weight. Also, it frequently and rapidly leads to normalization of glucose tolerance even before the onset of body weight reduction. The underlying mechanisms are yet unclear. In this study we aim to explore the mechanisms underlying the onset of insulin resistance and steatohepatitis in patients with steatosis and to identify the mechanisms leading to improved glucose tolerance in humans after bariatric surgery. We test the following hypotheses: increased lipid availability leads to (i) increased lipid oxidation and oxidative stress (ii) accumulation of lipid metabolites that impair insulin signalling (iii) bariatric surgery improves insulin sensitivity by increasing lipid oxidation.

This study will contribute to the understanding of MASLD and will help to identify new targets for the therapy of diabetes.

Interventions

  • Procedure surgery
    biliopancreatic diversion, gastric banding, gastric sleeve resection

Primary outcome measures

  • Energy metabolism [Time frame: 5 years]
Secondary outcome measures (2)
  • weight loss [Time frame: 5 years]
  • Insulin sensitivity [Time frame: 5 years]

Eligibility criteria

Inclusion criteria

  • Aged ≥ 20 years- ≤ 70 years
  • BMI 20- 25 kg/m 2 normal- weight group
  • BMI 35- 39,9 kg/m 2 (Obesity grade 2)
  • BMI >40 kg/m 2 (Obesity grade 3)

Exclusion criteria

  • Acute illness 2 weeks before start of examination
  • Autoimmune or Immune disorder diseases (Leukozyten < 5000/µl
  • Renal insufficiency (Kreatin > 1,5 mg/dl)
  • Heart disease, condition after heart attack
  • Anemia (Hb <12g/l, controlled before every day of examination) or blood donations 4weeks before examination.
  • Participation in another trial within the last 2 weeks
  • Pharmacological- immunotherapy (Cortisol, Antihistaminika, ASS)
  • Thyroid disorders
  • Glitazone Therapy
  • Pregnancy, Lactation, Menstruation
  • Smoking cigarettes, Alcohol- and drug abuse
  • Psychiatric disorders
  • Risk for/ or diagnosed HIV/ AIDS or Hepatitis B/C
  • Liver disease, which are not caused by non- alcoholic steato- hepatitis
  • Working on night shifts or irregular rhythm of night- day
  • Impaired wound healing or clotting disorders
  • Allergic reaction to local anesthetics
  • Malignant cancer

Criteria are shown verbatim from the registry (in English). Final eligibility is always assessed by the study center.

Healthy volunteers: Yes

Study design

Observational model
Case-control

Study locations

Germany · 1 center
  • German Diabetes Center — Düsseldorf

Publications

  • Koliaki C, Szendroedi J, Kaul K, Jelenik T, Nowotny P, Jankowiak F, Herder C, Carstensen M, Krausch M, Knoefel WT, Schlensak M, Roden M. Adaptation of hepatic mitochondrial function in humans with non-alcoholic fatty liver is lost in steatohepatitis. Cell Metab. 2015 May 5;21(5):739-46. doi: 10.1016/j.cmet.2015.04.004. PMID 25955209
  • Miya A, Tura A, Shokouhmehr A, Esposito I, Yavas A, Granderath FA, Schlensak M, Huttasch M, Xourafa G, Heilmann G, Kahl S, Roden M, Schrauwen P. Insulin resistance, not hepatic histological features, is the dominant correlate of insulin clearance in class 3 obesity. Diabetes Res Clin Pract. 2026 Aug 2:113481. doi: 10.1016/j.diabres.2026.113481. Online ahead of print. PMID 42543084
  • Kahl S, Strassburger K, Pacini G, Trinks N, Pafili K, Mastrototaro L, Dewidar B, Sarabhai T, Trenkamp S, Esposito I, Schlensak M, Granderath FA, Roden M. Dysglycemia and liver lipid content determine the relationship of insulin resistance with hepatic OXPHOS capacity in obesity. J Hepatol. 2025 Mar;82(3):417-426. doi: 10.1016/j.jhep.2024.08.012. Epub 2024 Aug 31. PMID 39218222
  • Kovac L, Gancheva S, Jahnert M, Sehgal R, Mastrototaro L, Schlensak M, Granderath FA, Rittig K, Roden M, Schurmann A, Kahl S, Ouni M. Different effects of bariatric surgery on epigenetic plasticity in skeletal muscle of individuals with and without type 2 diabetes. Diabetes Metab. 2024 Sep;50(5):101561. doi: 10.1016/j.diabet.2024.101561. Epub 2024 Jul 6. PMID 38977261
  • Sarabhai T, Kahl S, Gancheva S, Mastrototaro L, Dewidar B, Pesta D, Ratter-Rieck JM, Bobrov P, Jeruschke K, Esposito I, Schlensak M, Roden M. Loss of mitochondrial adaptation associates with deterioration of mitochondrial turnover and structure in metabolic dysfunction-associated steatotic liver disease. Metabolism. 2024 Feb;151:155762. doi: 10.1016/j.metabol.2023.155762. Epub 2023 Dec 19. PMID 38122893
  • Pafili K, Kahl S, Mastrototaro L, Strassburger K, Pesta D, Herder C, Putzer J, Dewidar B, Hendlinger M, Granata C, Saatmann N, Yavas A, Gancheva S, Heilmann G, Esposito I, Schlensak M, Roden M. Mitochondrial respiration is decreased in visceral but not subcutaneous adipose tissue in obese individuals with fatty liver disease. J Hepatol. 2022 Dec;77(6):1504-1514. doi: 10.1016/j.jhep.2022.08.010. Ep PMID 35988689
  • Apostolopoulou M, Gordillo R, Koliaki C, Gancheva S, Jelenik T, De Filippo E, Herder C, Markgraf D, Jankowiak F, Esposito I, Schlensak M, Scherer PE, Roden M. Specific Hepatic Sphingolipids Relate to Insulin Resistance, Oxidative Stress, and Inflammation in Nonalcoholic Steatohepatitis. Diabetes Care. 2018 Jun;41(6):1235-1243. doi: 10.2337/dc17-1318. Epub 2018 Mar 30. PMID 29602794

Identifiers

NCT: NCT01477957 · BARIA-DDZ

Primary sources (government registries)

View this study on ClinicalTrials.gov ↗