Metabolism

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Regulation of the glutamate dehydrogenase activity in rat islets of Langerhans and its consequence on insulin release
Metabolism - Tập 43 - Trang 1187-1195 - 1994
Jadwiga Bryla, Mariusz Michalik, June Nelson, Maria Erecińska
Lower androgenicity is associated with higher plasma levels of prothrombotic factors irrespective of age, obesity, body fat distribution, and related metabolic parameters in men
Metabolism - Tập 46 - Trang 1287-1293 - 1997
Giovanni De Pergola, Vito De Mitrio, Marcello Sciaraffia, Nicola Pannaccuilli, Antonio Minenna, Francesco Giorgino, Mariella Petronelli, Ester Laudadio, Riccardo Giorgino
Effect of angiotensin-converting enzyme inhibition with perindopril and β-blockade with atenolol on retinal blood flow in hypertensive diabetic subjects
Metabolism - Tập 47 - Trang 28-33 - 1998
V. Patel, S.M.B. Rassam, H.C. Chen, M. Jones, E.M. Kohner
Basal peroxisome proliferator activated receptor gamma coactivator 1α expression is independent of calcineurin in skeletal muscle
Metabolism - Tập 61 - Trang 389-394 - 2012
Sébastien Banzet, Hervé Sanchez, Rachel Chapot, André Peinnequin, Xavier Bigard, Nathalie Koulmann
Diisopropylammonium dichloroacetate: Regulation of metabolic intermediates in muscle of alloxan diabetic rats
Metabolism - Tập 20 - Trang 830-834 - 1971
Peter W. Stacpoole, James M. Felts
Hexokinase isozymes of normal human subcutaneous adipose tissue
Metabolism - Tập 27 - Trang 1101-1108 - 1978
Victor R. Lavis
β-cell function during insulin-modified intravenous glucose tolerance test successfully assessed by the C-peptide minimal model
Metabolism - Tập 48 - Trang 1162-1166 - 1999
Gianna Toffolo, William T. Cefalu, Claudio Cobelli
Increased insulin sensitivity and decreased insulin secretion in offspring of insulin-sensitive type 2 diabetic patients
Metabolism - Tập 49 - Trang 1219 - 2000
Miyake Seibei, Matsumoto Kazunari, Sakamaki Hiroyuki, Izumino Kiyohiro, Yano Mayumi, Ueki Yukitaka, Tominaga Yuko
To investigate the early defects of glucose metabolism in insulin-sensitive type 2 diabetes, we performed oral and frequently sampled intravenous glucose tolerance tests (OGTT and FSIGT) with minimal model analysis in 15 offspring of Japanese type 2 diabetics with normal insulin sensitivity (insulin resistance index of homeostasis model assessment [HOMA-R] < 2.0) and in 20 healthy control subjects without a family history of type 2 diabetes. The frequency of impaired glucose tolerance (IGT) was 40% (6 of 15) in the offspring and 0% (0 of 20) in the controls. Fasting plasma glucose (4.8 ± 0.1 v 4.6 ± 0.1 mmol/L, P = .18) and immunoreactive insulin ([IRI] 29.9 ± 2.5 v 28.3 ± 2.5 pmol/L, P ± = .64) were comparable between the offspring and the controls. The rate of glucose disappearance (KG) was significantly lower in the offspring versus the control group (2.00 ± 0.22 v 2.60 ± 0.17 min−1, P = .03). The insulin sensitivity index (Si) was significantly greater in the offspring versus the controls (2.68 ± 0.41 v 1.71 ± 0.17 × 10−4 · min−1 · pmol/L, P = .02). First-phase insulin secretion (FPI) to intravenous glucose was significantly lower in the offspring versus the control group (886 ± 110 v 2,296 ± 267 min · pmol/L, P < .01). Glucose effectiveness (SG) was comparable between the offspring and control groups. The disposition index (Si × FPI) was significantly lower in the offspring versus the controls (2,106 ± 256 v 3,652 ± 490 × 10−4, P = .02). When the offspring were subdivided into 2 groups by glucose tolerance status, both normal glucose tolerance (NGT) offspring and IGT offspring showed a significant decrease in FPI and increase in Si. Thus, although the offspring of insulin-sensitive type 2 diabetics had increased insulin sensitivity, the impairment in insulin secretion was more dominant. Our results suggest that the early metabolic abnormality in insulin-sensitive type 2 diabetes is an insulin secretory dysfunction despite increased insulin sensitivity.
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