Early metabolic defects in Arab subjects with strong family history of Type 2 diabetes

Journal of Endocrinological Investigation

Volumn 36, Issue 6, 2013, Pages 417-421

  Shalata, A ^a   Jazmawi, W ^b   Aslan, O ^b   Badarni, K ^a   Dabbah, K ^a   Sawaed, S ^b   Cohen Castel, O ^b   Borochowitz, Z U ^a   Karkabi, K ^b   DeFronzo, R ^c   Abdul Ghani, M ^c  

^a BNAI ZION MEDICAL CENTER   (Israel)

^b TECHNION ISRAEL INSTITUTE OF TECHNOLOGY   (Israel)

^c UNIVERSITY OF TEXAS HEALTH SCIENCE CENTER AT SAN ANTONIO   (United States)

Author keywords

Beta cell dysfunction; Family history of type 2 diabetes; Insulin resistance

Indexed keywords

FATTY ACID; GLUCOSE; INSULIN;

ADULT; ARAB; ARTICLE; CELL FUNCTION; CONTROLLED STUDY; FATTY ACID BLOOD LEVEL; FEMALE; GLUCOSE BLOOD LEVEL; GLUCOSE TOLERANCE; HUMAN; INSULIN RESISTANCE; INSULIN SENSITIVITY; MAJOR CLINICAL STUDY; MALE; METABOLIC DISORDER; NON INSULIN DEPENDENT DIABETES MELLITUS; ORAL GLUCOSE TOLERANCE TEST; PANCREAS ISLET BETA CELL;

ADULT; ARABS; BLOOD GLUCOSE; DIABETES MELLITUS, TYPE 2; EARLY DIAGNOSIS; FAMILY HEALTH; FASTING; FEMALE; GENETIC PREDISPOSITION TO DISEASE; GLUCOSE TOLERANCE TEST; HUMANS; INSULIN; INSULIN RESISTANCE; MALE; METABOLIC DISEASES; PEDIGREE;

EID: 84881459523     PISSN: 03914097     EISSN: 17208386     Source Type: Journal    
DOI: 10.3275/8762     Document Type: Article

References (13)

1. DeFronzo RA. Pathogenesis of type 2 diabetes mellitus. Med Clin North Am 2004, 88: 787-835.
2. Abdul-Ghani MA, DeFronzo RA. Pathophysiology of prediabetes. Curr Diab Rep 2009, 9: 193-9.
3. Abdul-Ghani MA, Tripathy D, DeFronzo RA. Contribution of beta cell dysfunction and insulin resistance to the pathogenesis of impaired glucose tolerance and impaired fasting glucose. Diabetes Care 2006, 29: 1130-9.
4. Abdul-Ghani MA, Jenkinson C, Richardson D, DeFronzo RA. Insulin secretion and insulin action in subjects with impaired fasting glucose and impaired glucose tolerance: results from the Veterans Administration Genetic Epidemiology Study (VEGAS). Diabetes 2006, 55: 1430-5.
5. Groop LC, Bonadonna RC, Del Prato S, et al. Glucose and free fatty acid metabolism in non-insulin-dependent diabetes mellitus. Evidence for multiple sites of insulin resistance. J Clin Invest 1989, 84: 205-13.
6. Petersen KF, Dufour S, Befroy D, et al. Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes. N Engl J Med 2004, 350: 664-71.
7. Kashyap SR, Belfort R, Berria R, et al. Discordant effects of a chronic physiological increase in plasma FFA on insulin signaling in healthy subjects with or without a family history of type 2 diabetes. Am J Physiol Endocrinol Metab 2004, 287: E537-46.
8. Pimenta W, Korytkowski M, Mitrakou A, et al. Pancreatic beta-cell dysfunction as the primary genetic lesion in NIDDM. Evidence from studies in normal glucose-tolerant individuals with a first-degree NIDDM relative. JAMA 1995, 273: 1855-61.
9. Doria A, Patti ME, Kahn CR. The emerging genetic architecture of type 2 diabetes. Cell Metab 2008, 8: 186-200.
10. Abdul-Ghani MA, Matsuda M, Balas B, DeFronzo RA. Muscle and liver insulin resistance indexes derived from the oral glucose tolerance test. Diabetes Care 2007, 30: 89-94.
11. Abdul-Ghani MA, Molina-Carrion M, Jani R, Jenkinson C, Defronzo RA. Adipocytes in subjects with impaired fasting glucose and impaired glucose tolerance are resistant to the anti-lipolytic effect of insulin. Acta Diabetol 2008, 45: 147-50.
12. Abdul-Ghani MA, DeFronzo RA. Pathogenesis of insulin resistance in skeletal muscle. J Biomed Biotechnol 2010, doi:10.1155/2010/476279
13. Ferrannini E, Bjorkman O, Reichard GA jr, et al. The disposal of an oral glucose load in healthy subjects. A quantitative study. Diabetes 1985, 34: 580-8.