Insulin resistance in normal rats infused with glucose for 72 h - PubMed (original) (raw)
Insulin resistance in normal rats infused with glucose for 72 h
S R Hager et al. Am J Physiol. 1991 Mar.
Abstract
Insulin resistance is accentuated during periods of poor metabolic control in human non-insulin-dependent diabetes mellitus. The role of hyperglycemia in this suppression of insulin action is not clear. If glucose impairs insulin action, then the effect should be reproducible in vivo in tissues of normal intact rats. To test this possibility, normal rats were continuously administered 50% glucose in water (60-66 mg.kg-1.min-1) via an indwelling jugular catheter. After 72 h, these animals were hyperglycemic, hyperinsulinemic, and glucosuric compared with control rats infused for 72 h with normal saline (P less than 0.01). Basal glucose uptake in vivo was greater in muscle of glucose-infused rats. Insulin-stimulated glucose uptake in vivo and in vitro (by perfused hindquarters and isolated adipocytes) were suppressed in the glucose-infused group (P less than 0.01). Glycogen synthase activity was reduced 40% in extracts of muscle and adipose tissue of hyperglycemic rats. Basal and isoproterenol-stimulated lipolysis were increased, whereas insulin suppression of lipolysis was blunted in adipocytes from glucose-infused animals (P less than 0.01). Glucose infusion did not alter insulin binding by isolated adipocytes or solubilized skeletal muscle insulin receptors. These results suggest that a 72-h in vivo glucose infusion impaired insulin action in muscle and adipose tissue of normal rats by inducing postbinding defects similar to those observed in human diabetes mellitus during intervals of deteriorated metabolic control.
Similar articles
- Glucose infusion causes insulin resistance in skeletal muscle of rats without changes in Akt and AS160 phosphorylation.
Hoy AJ, Bruce CR, Cederberg A, Turner N, James DE, Cooney GJ, Kraegen EW. Hoy AJ, et al. Am J Physiol Endocrinol Metab. 2007 Nov;293(5):E1358-64. doi: 10.1152/ajpendo.00133.2007. Epub 2007 Sep 4. Am J Physiol Endocrinol Metab. 2007. PMID: 17785505 - Activation of the hexosamine pathway by glucosamine in vivo induces insulin resistance in multiple insulin sensitive tissues.
Virkamäki A, Daniels MC, Hämäläinen S, Utriainen T, McClain D, Yki-Järvinen H. Virkamäki A, et al. Endocrinology. 1997 Jun;138(6):2501-7. doi: 10.1210/endo.138.6.5172. Endocrinology. 1997. PMID: 9165041
Cited by
- Combined Hyperglycemia- and Hyperinsulinemia-Induced Insulin Resistance in Adipocytes Is Associated With Dual Signaling Defects Mediated by PKC-ζ.
Lu H, Bogdanovic E, Yu Z, Cho C, Liu L, Ho K, Guo J, Yeung LSN, Lehmann R, Hundal HS, Giacca A, Fantus IG. Lu H, et al. Endocrinology. 2018 Apr 1;159(4):1658-1677. doi: 10.1210/en.2017-00312. Endocrinology. 2018. PMID: 29370351 Free PMC article. - Ginsenoside Rb1 and compound K improve insulin signaling and inhibit ER stress-associated NLRP3 inflammasome activation in adipose tissue.
Chen W, Wang J, Luo Y, Wang T, Li X, Li A, Li J, Liu K, Liu B. Chen W, et al. J Ginseng Res. 2016 Oct;40(4):351-358. doi: 10.1016/j.jgr.2015.11.002. Epub 2015 Nov 27. J Ginseng Res. 2016. PMID: 27746687 Free PMC article. - Nutrient Excess and AMPK Downregulation in Incubated Skeletal Muscle and Muscle of Glucose Infused Rats.
Coughlan KA, Balon TW, Valentine RJ, Petrocelli R, Schultz V, Brandon A, Cooney GJ, Kraegen EW, Ruderman NB, Saha AK. Coughlan KA, et al. PLoS One. 2015 May 21;10(5):e0127388. doi: 10.1371/journal.pone.0127388. eCollection 2015. PLoS One. 2015. PMID: 25996822 Free PMC article. - Insulin receptor signaling in normal and insulin-resistant states.
Boucher J, Kleinridders A, Kahn CR. Boucher J, et al. Cold Spring Harb Perspect Biol. 2014 Jan 1;6(1):a009191. doi: 10.1101/cshperspect.a009191. Cold Spring Harb Perspect Biol. 2014. PMID: 24384568 Free PMC article. Review. - A model of chronic nutrient infusion in the rat.
Fergusson G, Ethier M, Zarrouki B, Fontés G, Poitout V. Fergusson G, et al. J Vis Exp. 2013 Aug 14;(78):50267. doi: 10.3791/50267. J Vis Exp. 2013. PMID: 23979115 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical
Miscellaneous