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Long-term intermittent feeding, but not caloric restriction, leads to redox imbalance, insulin receptor nitration, and glucose intolerance.
Free Radic Biol Med. 2011 Oct 01; 51(7):1454-60.FR

Abstract

Calorie restriction is a dietary intervention known to improve redox state, glucose tolerance, and animal life span. Other interventions have been adopted as study models for caloric restriction, including nonsupplemented food restriction and intermittent, every-other-day feedings. We compared the short- and long-term effects of these interventions to ad libitum protocols and found that, although all restricted diets decrease body weight, intermittent feeding did not decrease intra-abdominal adiposity. Short-term calorie restriction and intermittent feeding presented similar results relative to glucose tolerance. Surprisingly, long-term intermittent feeding promoted glucose intolerance, without a loss in insulin receptor phosphorylation. Intermittent feeding substantially increased insulin receptor nitration in both intra-abdominal adipose tissue and muscle, a modification associated with receptor inactivation. All restricted diets enhanced nitric oxide synthase levels in the insulin-responsive adipose tissue and skeletal muscle. However, whereas calorie restriction improved tissue redox state, food restriction and intermittent feedings did not. In fact, long-term intermittent feeding resulted in largely enhanced tissue release of oxidants. Overall, our results show that restricted diets are significantly different in their effects on glucose tolerance and redox state when adopted long-term. Furthermore, we show that intermittent feeding can lead to oxidative insulin receptor inactivation and glucose intolerance.

Authors+Show Affiliations

Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, SP, BrazilNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21816219

Citation

Cerqueira, Fernanda M., et al. "Long-term Intermittent Feeding, but Not Caloric Restriction, Leads to Redox Imbalance, Insulin Receptor Nitration, and Glucose Intolerance." Free Radical Biology & Medicine, vol. 51, no. 7, 2011, pp. 1454-60.
Cerqueira FM, da Cunha FM, Caldeira da Silva CC, et al. Long-term intermittent feeding, but not caloric restriction, leads to redox imbalance, insulin receptor nitration, and glucose intolerance. Free Radic Biol Med. 2011;51(7):1454-60.
Cerqueira, F. M., da Cunha, F. M., Caldeira da Silva, C. C., Chausse, B., Romano, R. L., Garcia, C. C., Colepicolo, P., Medeiros, M. H., & Kowaltowski, A. J. (2011). Long-term intermittent feeding, but not caloric restriction, leads to redox imbalance, insulin receptor nitration, and glucose intolerance. Free Radical Biology & Medicine, 51(7), 1454-60. https://doi.org/10.1016/j.freeradbiomed.2011.07.006
Cerqueira FM, et al. Long-term Intermittent Feeding, but Not Caloric Restriction, Leads to Redox Imbalance, Insulin Receptor Nitration, and Glucose Intolerance. Free Radic Biol Med. 2011 Oct 1;51(7):1454-60. PubMed PMID: 21816219.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Long-term intermittent feeding, but not caloric restriction, leads to redox imbalance, insulin receptor nitration, and glucose intolerance. AU - Cerqueira,Fernanda M, AU - da Cunha,Fernanda M, AU - Caldeira da Silva,Camille C, AU - Chausse,Bruno, AU - Romano,Renato L, AU - Garcia,Camila C M, AU - Colepicolo,Pio, AU - Medeiros,Marisa H G, AU - Kowaltowski,Alicia J, Y1 - 2011/07/21/ PY - 2011/06/06/received PY - 2011/07/08/accepted PY - 2011/8/6/entrez PY - 2011/8/6/pubmed PY - 2011/12/31/medline SP - 1454 EP - 60 JF - Free radical biology & medicine JO - Free Radic Biol Med VL - 51 IS - 7 N2 - Calorie restriction is a dietary intervention known to improve redox state, glucose tolerance, and animal life span. Other interventions have been adopted as study models for caloric restriction, including nonsupplemented food restriction and intermittent, every-other-day feedings. We compared the short- and long-term effects of these interventions to ad libitum protocols and found that, although all restricted diets decrease body weight, intermittent feeding did not decrease intra-abdominal adiposity. Short-term calorie restriction and intermittent feeding presented similar results relative to glucose tolerance. Surprisingly, long-term intermittent feeding promoted glucose intolerance, without a loss in insulin receptor phosphorylation. Intermittent feeding substantially increased insulin receptor nitration in both intra-abdominal adipose tissue and muscle, a modification associated with receptor inactivation. All restricted diets enhanced nitric oxide synthase levels in the insulin-responsive adipose tissue and skeletal muscle. However, whereas calorie restriction improved tissue redox state, food restriction and intermittent feedings did not. In fact, long-term intermittent feeding resulted in largely enhanced tissue release of oxidants. Overall, our results show that restricted diets are significantly different in their effects on glucose tolerance and redox state when adopted long-term. Furthermore, we show that intermittent feeding can lead to oxidative insulin receptor inactivation and glucose intolerance. SN - 1873-4596 UR - https://www.unboundmedicine.com/medline/citation/21816219/Long_term_intermittent_feeding_but_not_caloric_restriction_leads_to_redox_imbalance_insulin_receptor_nitration_and_glucose_intolerance_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0891-5849(11)00447-3 DB - PRIME DP - Unbound Medicine ER -