Abstract
Background
Short time overfeeding of rats rapidly leads to insulin resistance (IR). A study with healthy human volunteers, which we suggest are less susceptible for developing IR after short time overfeeding, did not show these effects on IR. Therefore a study population of weight-stable, former morbidly obese subjects (BMI 31.3 kg/m2), which were treated with bariatric surgery approximately 3 years ago was selected.
Methods
Eleven subjects were submitted to a 7-day overfeeding study, resulting in a 53% increase in caloric intake (1,227 ± 394.4 to 1,879.2 ± 298.4 kcal/day). During normal diet and after overfeeding, insulin sensitivity was measured using steady state plasma glucose (SSPG) levels. At these time points, BMI and waist/hip ratio together with plasma levels of inflammatory markers (CRP, AGP, LBP, and TNF-α receptors) and plasma leptin values were also measured.
Results
SSPG levels after overfeeding increased from 8.2 ± 3.2 to 10.6 ± 2.6 mmol/l (P < 0.05), indicating decreased insulin sensitivity after overfeeding. Fasting plasma insulin, glucose, circulating levels of inflammatory markers, BMI, and waist/hip ratio remained unchanged.
Conclusions
This study shows that overfeeding in a group of weight-stable, former morbidly obese subjects 3 years after bariatric surgery results in decreased insulin sensitivity. The mechanisms behind decreased insulin sensitivity induced by overfeeding are poorly understood, but the present results reveal that a unique human model is available to study these mechanisms, leading to a better understanding of the pathophysiology of IR.
Similar content being viewed by others
References
Cottam DR, Mattar SG, Barinas-Mitchell E, et al. The chronic inflammatory hypothesis for the morbidity associated with morbid obesity: implications and effects of weight loss. Obes Surg. 2004;14:589–600.
Wang J, Obici S, Morgan K, et al. Overfeeding rapidly induces leptin and insulin resistance. Diabetes. 2001;50:2786–91.
Ohannesian JP, Marco CC, Najm PS, et al. Small weight gain is not associated with development of insulin resistance in healthy, physically active individuals. Horm Metab Res. 1999;31:323–5.
Guidone C, Manco M, Valera-Mora E, et al. Mechanisms of recovery from type 2 diabetes after malabsorptive bariatric surgery. Diabetes. 2006;55:2025–31.
Reaven GM, Silvers A, Farquhar JW. Study of the relationship between plasma insulin concentration and efficiency of glucose uptake in normal and mildly diabetic subjects. Diabetes. 1970;19:571–8.
Shen SW, Reaven GM, Farquhar JW. Comparison of impedance to insulin-mediated glucose uptake in normal subjects and in subjects with latent diabetes. J Clin Invest. 1970;49:2151–60.
Pei D, Jones CN, Bhargava R, et al. Evaluation of octreotide to assess insulin-mediated glucose disposal by the insulin suppression test. Diabetologia. 1994;37:843–5.
van Dielen FM, Buurman WA, Hadfoune M, et al. Macrophage inhibitory factor, plasminogen activator inhibitor-1, other acute phase proteins, and inflammatory mediators normalize as a result of weight loss in morbidly obese subjects treated with gastric restrictive surgery. J Clin Endocrinol Metab. 2004;89:4062–8.
Mott DM, Lillioja S, Bogardus C. Overnutrition induced decrease in insulin action for glucose storage: in vivo and in vitro in man. Metabolism. 1986;35:160–5.
Dhindsa S, Tripathy D, Mohanty P, et al. Differential effects of glucose and alcohol on reactive oxygen species generation and intranuclear nuclear factor-kappaB in mononuclear cells. Metabolism. 2004;53:330–4.
Mohanty P, Hamouda W, Garg R, et al. Glucose challenge stimulates reactive oxygen species (ROS) generation by leucocytes. J Clin Endocrinol Metab. 2000;85:2970–3.
Mohanty P, Ghanim H, Hamouda W, et al. Both lipid and protein intakes stimulate increased generation of reactive oxygen species by polymorphonuclear leukocytes and mononuclear cells. Am J Clin Nutr. 2002;75:767–72.
Houstis N, Rosen ED, Lander ES. Reactive oxygen species have a causal role in multiple forms of insulin resistance. Nature. 2006;440:944–8.
Rutkowski DT, Kaufman RJ. A trip to the ER: coping with stress. Trends Cell Biol. 2004;14:20–8.
Harding HP, Zhang Y, Zeng H, et al. An integrated stress response regulates amino acid metabolism and resistance to oxidative stress. Mol Cell. 2003;11:619–33.
Ozcan U, Cao Q, Yilmaz E, et al. Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes. Science. 2004;306:457–61.
Chin-Chance C, Polonsky KS, Schoeller DA. Twenty-four-hour leptin levels respond to cumulative short-term energy imbalance and predict subsequent intake. J Clin Endocrinol Metab. 2000;85:2685–91.
Hansen EN, Torquati A, Abumrad NN. Results of bariatric surgery. Annu Rev Nutr. 2006;26:481–511.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Nijhuis, J., van Dielen, F.M.H., Schaper, N.C. et al. Short-term Overfeeding Induces Insulin Resistance in Weight-stable Patients After Bariatric Surgery. OBES SURG 18, 300–305 (2008). https://doi.org/10.1007/s11695-007-9306-9
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s11695-007-9306-9