A Low Glycemic Index Diet as Prevention of the Catch-up Fat Phenomenon

University of Kiel

Status: Completed

Conditions: Dietary Intervention

Treatments: Other: dietary intervention by varying GI diets

Study type: Interventional

Funder types: Other

Identifiers

NCT01737034

BMBF 0315681

Details and patient eligibility

About

The catch-up fat phenomenon is an evolutionary conserved physiological response to a starvationrefeeding cycle. It is characterized by long-term suppression of thermogenesis, reduced body protein regain and an increase in fat mass above basal level during refeeding. Clinically, it characterises weight cycling in overweight patients which is associated with increasing fat mass (visceral fat) and increased morbidity (e.g. insulin resistance, inflammation). In this project, the physiological, cellular and molecular mechanisms of this phenomenon will be investigated in humans, mice and C. elegans. It is hypothesized that refeeding a low GI (=glycemic index)- diet after weight loss prevents the catchup fat phenomenon and its sequelae. This translational research will provide comprehensive insights into the catch-up fat phenomenon as well as provide a suitable strategy of its prevention.

Full description

In a human intervention study, changes in physiological, metabolic, and neuroendocrine functions in response to weight cycling will be investigated under controlled conditions in normal weight subjects. The mechanisms of the catch-up fat phenomenon are analysed starting from stable energy balance followed by overfeeding, weight loss and weight regain following weight loss (refeeding). Changes in body composition (including ectopic fat), metabolism (resting energy expenditure, substrate oxidation rates, insulin resistance) and plasma hormone concentrations will be assessed. Fat tissue probes will be used to characterise key enzymes and signalling pathways, redox status and whole genome expression. Modulation of the hormonal response to weight cycling is brought about by varying macronutrient content and glycemic index of the diets. We hypothesize that, insulin and leptin resistance are explained by increased insulin secretion during the refeeding period. Both, adaptive thermogenesis as well as insulin and leptin resistance can be ameliorated by attenuation of the increase in insulin and leptin secretion during refeeding a low GI diet after weight loss.

Enrollment: 32 patients

Sex: Male

Ages: 20 to 40 years old

Volunteers: Accepts Healthy Volunteers

Inclusion criteria

• normal weight (BMI 20-24 kg/m2), normal fat mass

Exclusion criteria

• smoking, chronic diseases, drug intake, nutrient allergies, lactose intolerance, pacemaker, metalliferous implants

Trial design

Primary purpose: Prevention

Allocation: Randomized

Interventional model: Parallel Assignment

Masking: None (Open label)

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32 participants in 4 patient groups

low GI, low GI

Experimental group

Description:

low GI diet (semi starvation phase) followed by low GI diet in the refeeding phase

Treatment:

Other: dietary intervention by varying GI diets

low GI, high GI

Experimental group

Description:

low GI diet (semi starvation phase) followed by high GI diet in the refeeding phase

Treatment:

Other: dietary intervention by varying GI diets

high GI, low GI

Experimental group

Description:

high GI diet (semi starvation phase) followed by low GI diet in the refeeding phase

Treatment:

Other: dietary intervention by varying GI diets

high GI, high GI

Experimental group

Description:

high GI diet (semi starvation phase) followed by high GI diet in the refeeding phase

Treatment:

Other: dietary intervention by varying GI diets