The disposal of an oral glucose load in patients with non-insulin-dependent diabetes - PubMed (original) (raw)
Comparative Study
The disposal of an oral glucose load in patients with non-insulin-dependent diabetes
E Ferrannini et al. Metabolism. 1988 Jan.
Abstract
Following glucose ingestion, tissue glucose uptake is enhanced and endogenous glucose production is inhibited, thus contributing to the maintenance of normal glucose tolerance. To examine whether these responses are disturbed in diabetes, glucose kinetics after oral glucose administration were studied in 12 non-insulin-dependent diabetic and 10 age- and weight-matched control subjects. A double tracer approach was used, whereby the endogenous glucose pool was labeled with 3-3H-glucose and the oral load with 1-14C-glucose. The two glucose tracers were separated in plasma by a two-step chromatographic procedure, and the two sets of isotopic data were analyzed according to a two-compartment model for the glucose system. Basally, glucose production was slightly higher in diabetics than in controls (2.51 +/- 0.24 v 2.28 +/- 0.11 mg/kg.min, NS) even though the former had higher plasma glucose (189 +/- 19 v 93 +/- 2 mg/dL, P less than .001) and insulin (23 +/- 4 v 12 +/- 1 microU/mL, P less than .05) concentrations. Following the ingestion of 1 g/kg of glucose, oral glucose appeared in the peripheral circulation in similar time-course and amount in the two groups (75 +/- 2% of the load over 3.5 hours in the diabetics v 76 +/- 3% in controls). Endogenous glucose production was promptly inhibited in diabetic and normal subjects alike, but the mean residual hepatic glucose production after glucose ingestion was significantly greater in the diabetic group (17 +/- 2 v 10 +/- 3 g/3.5 h, P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
Similar articles
- Glucose fluxes and oxidation after an oral glucose load in patients with non-insulin-dependent diabetes mellitus of variable severity.
Féry F, Melot C, Balasse EO. Féry F, et al. Metabolism. 1993 Apr;42(4):522-30. doi: 10.1016/0026-0495(93)90113-3. Metabolism. 1993. PMID: 8487677 - The disposal of an oral glucose load in healthy subjects. A quantitative study.
Ferrannini E, Bjorkman O, Reichard GA Jr, Pilo A, Olsson M, Wahren J, DeFronzo RA. Ferrannini E, et al. Diabetes. 1985 Jun;34(6):580-8. doi: 10.2337/diab.34.6.580. Diabetes. 1985. PMID: 3891471 - On the role of the gut in diabetic hyperglucagonaemia.
Lund A. Lund A. Dan Med J. 2017 Apr;64(4):B5340. Dan Med J. 2017. PMID: 28385175 Review.
Cited by
- The human genetic variant rs6190 unveils Foxc1 and Arid5a as novel pro-metabolic targets of the glucocorticoid receptor in muscle.
Prabakaran AD, Chung HJ, McFarland K, Govindarajan T, El Abdellaoui Soussi F, Durumutla HB, Villa C, Piczer K, Latimer H, Werbrich C, Akinborewa O, Horning R, Quattrocelli M. Prabakaran AD, et al. bioRxiv [Preprint]. 2024 Mar 31:2024.03.28.586997. doi: 10.1101/2024.03.28.586997. bioRxiv. 2024. PMID: 38585940 Free PMC article. Preprint. - A Narrative Review on Strategies for the Reversion of Prediabetes to Normoglycemia: Food Pyramid, Physical Activity, and Self-Monitoring Innovative Glucose Devices.
Rondanelli M, Barrile GC, Cavioni A, Donati P, Genovese E, Mansueto F, Mazzola G, Patelli Z, Pirola M, Razza C, Russano S, Sivieri C, Tartara A, Valentini EM, Perna S. Rondanelli M, et al. Nutrients. 2023 Nov 28;15(23):4943. doi: 10.3390/nu15234943. Nutrients. 2023. PMID: 38068801 Free PMC article. Review. - Role of Dgat2 in Glucose Uptake and Fatty Acid Metabolism in C2C12 Skeletal Myotubes.
Bu SY. Bu SY. J Microbiol Biotechnol. 2023 Dec 28;33(12):1563-1575. doi: 10.4014/jmb.2307.07018. Epub 2023 Aug 18. J Microbiol Biotechnol. 2023. PMID: 37644753 Free PMC article. - Efferocytosis: An Emerging Therapeutic Strategy for Type 2 Diabetes Mellitus and Diabetes Complications.
Liu X, Liu H, Deng Y. Liu X, et al. J Inflamm Res. 2023 Jul 7;16:2801-2815. doi: 10.2147/JIR.S418334. eCollection 2023. J Inflamm Res. 2023. PMID: 37440994 Free PMC article. Review. - Myofiber Baf60c controls muscle regeneration by modulating Dkk3-mediated paracrine signaling.
Xu J, Li X, Chen W, Zhang Z, Zhou Y, Gou Y, Lv CA, Jin L, Qiu X, Ma S, Wu QQ, Liu T, Mi L, Yang Z, Yu T, Pan X, Feng Y, Shan P, Meng ZX. Xu J, et al. J Exp Med. 2023 Sep 4;220(9):e20221123. doi: 10.1084/jem.20221123. Epub 2023 Jun 7. J Exp Med. 2023. PMID: 37284884 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Miscellaneous