http://www.cnr.it/ontology/cnr/individuo/prodotto/ID23731

Beta cell function in morbidity obese subject free liver: long-term effectof weight loss (Articolo in rivista)

Type

Prodotto della ricerca (Classe)
Articolo in rivista (Classe)

Label

Beta cell function in morbidity obese subject free liver: long-term effectof weight loss (Articolo in rivista) (literal)

Anno

2005-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

10.2337/diabetes.54.8.2382 (literal)

Alternative label

Camastra S.; Manco M.; Mari A.; Baldi S.; Gastaldelli A.; Greco A.V.; Mingrone G.; Ferrannini E. (2005)
Beta cell function in morbidity obese subject free liver: long-term effectof weight loss
in Diabetes (N.Y.N.Y.)
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Camastra S.; Manco M.; Mari A.; Baldi S.; Gastaldelli A.; Greco A.V.; Mingrone G.; Ferrannini E. (literal)

Pagina inizio

2382 (literal)

Pagina fine

2389 (literal)

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http://diabetes.diabetesjournals.org/content/54/8/2382.full (literal)

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54 (literal)

Rivista

Diabetes (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note

In: \"Diabetes \"54,2005,8,2382-2389 (literal)

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8 (literal)

Note

ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

[1,4,5,8] Department of Internal Medicine, Metabolism Unit, National Research Council Institute of Clinical Physiology, University of Pisa, Pisa, Italy [2,6,7] Department of Medicine, Catholic University, Rome, Italy [3] National Research Council Institute of Biomedical Engineering, Padua, Italy (literal)

Titolo

Beta cell function in morbidity obese subject free liver: long-term effectof weight loss (literal)

Abstract

Abstract: Insulin hypersecretion and insulin resistance are physiologically linked features of obesity. We tested whether extreme hypersecretion impairs beta-cell function under free-living conditions and whether major weight loss modifies insulin hypersecretion, insulin sensitivity, and beta-cell function. Plasma glucose, C-peptide, and free fatty acid concentrations were measured at hourly intervals during 24 h of normal life (including calorie-standardized meals) in 20 morbidly obese nondiabetic patients (BMI 48.4 +/- 1.7 kg/m(2)) and 7 nonobese age- and sex-matched control subjects; 8 of the obese patients were restudied 6 months and 2 years following biliopancreatic diversion. Insulin secretion was reconstructed from C-peptide levels by deconvolution and related to concurrent glucose levels through a mathematical model incorporating key features of beta-cell function: rate sensitivity, beta-cell glucose sensitivity, and potentiation. Insulin sensitivity (by the euglycemic insulin clamp technique) was reduced by 50% in obese subjects (23.1 +/- 2.5 of obese subjects vs. 52.9 +/- 4.9 mu mol (.) min(-1) (.) kg(FFM)(-1) of control subjects, means +/- SE, P = 0.0004) as was mean 24-h insulin clearance (median 809 [interquartile range 451] vs. 1,553 [520] ml (.) min-(1) m(-2), P < 0.001) due to a 50% reduction in hepatic insulin extraction (P < 0.01). Over 24 h, insulin secretion was doubled in obese subjects (468 nmol [202] in obese subjects vs. 235 [85] of control subjects, P = 0.0002). Despite the hypersecretion, beta-cell glucose sensitivity, rate sensitivity, and potentiation were similar in obese and control subjects. Six months postoperatively (weight loss = 33 3 kg), both insulin hypersecretion (282 nmol [213]) and insulin sensitivity (51.6 +/- 3.7 mu mol (.) min(-1) (.) kg(FFM)(-1)) were normalized. At 2 years (weight loss = 50 8 kg), insulin sensitivitiy was supernormal (68.7 +/- 3.3 mu mol (.) min(-1) (.) kg(FFM)(-1)) and insulin secretion was lower than normal (167 nmol [37]) (both P < 0.05 vs. control subjects). In conclusion, severe uncomplicated obesity is characterized by gross insulin hypersecretion and insulin resistance, but the dynamic aspects of beta-cell function are intact. Malabsorptive bariatric surgery corrects both the insulin hypersecretion and the insulin resistance at a time when BMI is still high. With continued weight loss over a 2-year period, moderately obese subjects become supersensitive to insulin and, correspondingly, insulin hyposecretors. (literal)

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