Oral Presentation Australian & New Zealand Obesity Society 2015 Annual Scientific Meeting

Predictors of susceptibility to weight change during a single cycle of weight gain and loss (#31)

Amy T Hutchison 1 , Dorit Samocha-Bonet 2 , Leonie K Heilbronn 1 3
  1. Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia
  2. Diabetes and Metabolism, Garvan Institute of Medical Research, Sydney, NSW, Australia
  3. South Australian Health and Medical Research Institute (SAHMRI), Adelaide, SA, Australia

Weight-cycling  is associated with weight re-gain and type 2 diabetes.  We have previously shown inter-individual variability in weight gain following overfeeding. Variability is also observed following hypocaloric diets, and in weight loss success. What predisposes individuals to weight fluctuation is unclear, and may modulate disease risk. We examined metabolic changes in overweight individuals, during a single weight-cycling period. Nineteen overweight individuals (10 men/9 women; age: 37±12y, BMI: 28.3±2.4kg/m2) followed a hypercaloric diet (+1250kcal/d) for 28d, then switched to a liquid calorie diet (800kcal/d) for 12 weeks, or until they lost 10% body weight.  Body composition, fasting insulin, leptin, gastric inhibitory polypeptide (GIP), monocyte chemoattractant protein-1 (MCP-1) and CRP were assessed after overfeeding, and weight loss. 

Individuals gained 2.9±0.4kg (1.9±0.4kg fat) and lost 7.1±0.6kg (6.6±3.2kg fat) (all P<0.05).  Weight loss, and the time to lose 5% of initial body weight, were related to the amount of weight gained (r=0.62,r=0.71 respectively, both P<0.01).  Thus, we classified individuals as “diet-sensitive”(n=10; 4 men/6 women; BMI 29.2±0.8kg/m2) or “diet-resistant” (n=9; 6 men/3 women; BMI 27.3±0.6kg/m2).  Diet-sensitive individuals (those with the largest weight changes) gained, and lost, more abdominal and total body fat following overfeeding and weight loss (all P<0.05).

Overfeeding increased insulin, leptin, GIP, MCP-1 and CRP (P<0.05). Weight loss reduced insulin and leptin; the reduction in leptin was greater in diet-sensitive individuals (P<0.01). Following weight loss, GIP concentrations were reduced in diet-sensitive individuals only (P<0.05), whilst MCP-1 and CRP were unchanged in both groups.  Diet-sensitive individuals had higher baseline leptin and CRP concentrations (P<0.05).

Individuals who gained more weight also lost more weight, suggesting they were sensitive to dietary changes. Only leptin and CRP were related to this susceptibility. Weight gain increased CRP; this was not corrected by weight loss.  This may contribute to the increased risk of type 2 diabetes in weight-cycling individuals.