Obesity (Disorder), Obesity & Overweight
Conditions
Keywords
Weight loss, obesity, adipose tissue, inflammation, mitochondria, metabolism, conservative treatment of obesity, lifestyle intervention of obesity
Brief summary
This prospective observational study investigates weight loss and metabolic changes in adults with obesity undergoing standard clinical diet-induced lifestyle treatment and counseling. Participants follow a very-low-calorie diet followed by a conventional weight loss diet in addition to lifestyle counseling and are followed for 12 months. The study examines weight loss as the primary outcome and characterizes changes in body composition, fat distribution, glucose metabolism, inflammation, and adipose tissue biology as secondary outcomes.
Detailed description
Obesity is associated with metabolic complications including insulin resistance, fatty liver disease, dyslipidaemia, and systemic inflammation. Weight loss can improve these complications, yet individuals vary widely in weight loss, fat distribution and metabolic response. Subcutaneous adipose tissue dysfunction, including impaired mitochondrial biogenesis and increased inflammation, is thought to play a central role. This prospective observational study follows adults with obesity undergoing standard-of-care diet and lifestyle treatment at Helsinki University Central Hospital, Helsinki, Finland. The intervention consists of a very-low-calorie diet for approximately 10 weeks, followed by gradual transition to a conventional weight loss diet and multidisciplinary clinical follow-up. Assessments are performed at baseline, 6 months, and 12 months and include anthropometry, body composition (BIA, DXA), fasting blood samples, and oral glucose tolerance testing. Subcutaneous adipose tissue biopsies are obtained from four anatomical depots (gluteal, abdominal, breast, and upper arm) for molecular, mitochondrial, epigenetic, and histological analyses. The primary outcome is diet-induced weight loss over 12 months. Secondary outcomes include changes in fat distribution, insulin sensitivity, lipid profile, inflammation, mitochondrial measures in adipose tissue, and depot-specific adipose tissue characteristics.
Interventions
BEHAVIORALDiet-Induced Weight Loss Program
Standard clinical obesity treatment consisting of a very-low-calorie diet for approximately 10 weeks followed by transition to a conventional weight loss diet with multidisciplinary clinical follow-up.
Sponsors
University of Helsinki
Study design
Observational model
COHORT
Time perspective
PROSPECTIVE
Eligibility
Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No
Inclusion criteria
* Age ≥18 years * BMI ≥28 kg/m² * Seeking treatment for obesity at Helsinki University Central Hospital or affiliated units
Exclusion criteria
* Pregnancy or lactation * Current smoking * Anemia (Hb \<130 g/L in men; \<120 g/L in women) * Severe comorbid disease or condition judged by investigator to compromise safety * Contraindications to MRI (e.g., metal implants, claustrophobia)
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Percent Total Body Weight Loss (%TWL) | Baseline to 6 months | Percentage change in body weight from baseline, calculated as 100 × (baseline weight - follow-up weight) / baseline weight |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Change in Body Weight (kg) | Baseline to 6 and to 12 months | Absolute change in body weight measured in kilograms (kg). Reported as mean change from baseline. |
| Change in Total Body Fat Mass (kg) | Baseline to 6 months and to 12 months | Change in total body fat mass measured by body impedance analysis (BIA). Reported as mean change from baseline (kg). |
| Change in Body Fat percentage (%) | Baseline to 6 and to 12 months | Change in fat percentage measured by body impedance analysis (BIA). Reported as mean change from baseline (%). |
| Change in Plasma Glycated Hemoglobin (HbA1c) | Baseline to 6 months and to 12 months | HbA1c plasma glycated hemoglogin measured in SI units mmol/mol, Reported as mean change from baseline. |
| Change in HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) | Baseline to 6 and to 12 months | HOMA-IR calculated as fasting glucose (mmol/L) × fasting insulin (mU/L) / 22.5. Reported as mean change from baseline. |
| Change in Plasma Total Cholesterol (mmol/L) | Baseline to 6 months and to 12 months | Change in Plasma Total Cholesterol (mmol/L), Reported as mean change from baseline. |
| Change in Plasma LDL Cholesterol (mmol/L) | Baseline to 6 months and to 12 months | Change in Plasma LDL Cholesterol (mmol/L). Reported as mean change from baseline. |
| Change in Plasma HDL Cholesterol (mmol/L) | Baseline to 6 months and to 12 months | Change in HDL Cholesterol (mmol/L). Reported as mean change from baseline. |
| Change in Plasma Triglycerides (mmol/L) | Baseline to 6 months and to 12 months | Change in Plasma Triglycerides (mmol/L). Reported as mean change from baseline. |
| Change in Plasma C-Reactive Protein Concentration (mg/L) | Baseline, to 6 months and to 12 months | Change in Plasma high-sensitivity C-Reactive Protein Concentration (hs-CRP, mg/L). Reported as mean change from baseline. |
| Change in Mitochondrial DNA amount in Subcutaneous Abdominal Adipose Tissue | Baseline to 6 months and to 12 months | Change in Mitochondrial DNA Amount in Subcutaneous Abdominal Adipose Tissue, measured by qPCR as the ratio of mitochondrial to nuclear genes. Reported as a mean change from baseline. |
| Change in Mitochondrial DNA amount in Subcutaneous Breast Adipose Tissue | Baseline to 6 months and to 12 months | Change in Mitochondrial DNA Amount in Subcutaneous Breast Adipose Tissue, measured by qPCR as the ratio of mitochondrial to nuclear genes. Reported as a mean change from baseline. |
| Change in Mitochondrial DNA amount in Subcutaneous Upper Arm Adipose Tissue | Baseline to 6 months and to 12 months | Change in Mitochondrial DNA Amount in Subcutaneous Upper Arm Adipose Tissue, measured by qPCR as the ratio of mitochondrial to nuclear genes. Reported as a mean change from baseline. |
| Change in Mitochondrial DNA amount in Subcutaneous Lateral Upper Thigh Adipose Tissue | Baseline to 6 months and to 12 months | Change in Mitochondrial DNA Amount in Subcutaneous Lateral Upper Thigh Adipose Tissue, measured by qPCR as the ratio of mitochondrial to nuclear genes. Reported as a mean change from baseline. |
Outcome results
None listed