First phase insulin response in students of the University of Ibadan with family history of diabetes mellitus

Povzetek

Background: Impairment of the first phase of glucose-induced insulin secretion has long and repeatedly been recognized as an earliest detectable defect of β-cell function in individuals destined to develop type 2 diabetes mellitus. This study investigated the effect of positive family history of diabetes mellitus on the first phase insulin response in young adults.

Methodology: A cross-sectional study conducted among aged-matched 60 apparently healthy individuals, 30 with family history of diabetes among their 1st and or 2nd degree relatives (subjects) and 30 without family history of diabetes (controls). Glucose-oxidase method was used to assay serum glucose while serum insulin was assayed using Enzyme Linked Immunosorbent Assay. The insulin resistance index, insulin sensitivity index and B- cell function index was calculated using University of Oxford HOMA calculator, version 2.2 software. Statistical analysis was performed using SPSS version 17. Descriptive statistics, student’s t-test, Mann-Whitney U- test and Odds ratio were done.

Results: Results are expressed as mean (SD). Young adults with family history of diabetes mellitus had significantly higher first phase insulin concentration, fasting glucose concentration, fasting insulin concentration, insulin resistance index and β-cell function index than those without family history [p=0.006, 0.014, 0.004, 0.000 and 0.031 respectively]. The insulin sensitivity index was significantly lower in offspring of diabetics than in those of non-diabetics [p=0.001].

Conclusions: Young adults with family history of diabetes among relatives have higher risk of developing the disease than their counterpart without family history.

Keywords: First phase insulin response, family history, type 2 diabetes mellitus, young adult

Résumé

Contexte : La déficience de la première phase de la sécrétion d’insuline induite par le glucose a longtemps été reconnue comme l’un des premiers défauts détectables de la fonction des cellules βchez des individus destinés à développer un diabète sucré de type 2. Cette étude a examiné l’effet des antécédents familiaux positifs de diabète sucré sur la réponse insulinique de première phase chez les jeunes adultes.

Méthodologie : Une étude transversale réalisée parmi 60 personnesd’âge-appariés apparemment en bonne santé, 30 avec des antécédents familiaux de diabète parmi leurs relatifs de 1er et ou 2èmedegré (sujets) et 30 sans antécédents familiaux de diabète (contrôles). La méthode glucose-oxydase a été utilisée pour doser le glucose sérique, tandis que l’insuline sérique a été analysée à l’aide du dosage immunoadsorbant lié à l’enzyme. L’indice de résistance à l’insuline, l’indice de sensibilité à l’insuline et l’indice de fonction des cellules βont été  calculés à l’aide de la calculatrice HOMA de l’Université d’Oxford, version logiciel 2.2. L’analyse statistique a été réalisée à l’aide de SPSS version 17. Des statistiques descriptives, le test t de l’étudiant, le test U de Mann-Whitney et lerapport decotes ont été effectués.

Résultats : Les résultats sont exprimés en moyenne (DS). Les jeunes adultes ayant des antécédents familiaux de diabète sucré ont une concentration en insuline, une glycémie à jeun, une concentration en insuline à jeun, un indice de résistance à l’insuline et un indice de fonction des cellules βnettement supérieurs en première phase que ceux sans antécédents familiaux [p = 0,006, 0,014, 0,004, 0,000 et 0,031 respectivement]. L’indice de sensibilité à l’insuline était significativement plus faible parmi les enfants des diabétiques que de ceux non-diabétiques [p = 0,001].

Conclusions : Les jeunes adultes ayant des antécédents familiaux de diabète parmi les membres de leur famille ont un risque plus élevé de développer la maladie que leurs homologues sans
antécédents familiaux.

Mots-clés: réponse insulinique de première phase, antécédents familiaux, diabète sucré de type 2, jeune adulte

Correspondence: Dr. F.M. Abbiyesuku, Department of Chemical Pathology, College of Medicine, University of Ibadan, Ibadan, Nigeria. E-mail: fmabbiyesuku@yahoo.com

Literatura

Fagot-Campagna A, Pettitt DJ, Engelgau MM, et al. Type 2 diabetes among North American children and adolescents: an epidemiologic review and a public health perspective. J Pediatr. 2000; 136: 662–664.

Arslanian S. Type 2 diabetes in children: clinical aspects and risk factors. Horm Res. 2002; 57:19 –28.

Cherrington AD, Sindelar D, Edgerton D, Steiner K and McGuinness OP. Physiological consequences of phasic insulin release in the normal animal. Diabetes. 2002; 51 (Suppl. 1) :S103 –108

Godsland IF, Jeffs JAR and Johnston DC.. Loss of beta cell function as fasting glucose increases in the non-diabetic range. Diabetologia. 2004; 47:1157 –1166.

Thorens B. Neural regulation of pancreatic islet cell mass and function. Diabetes Obes Metab. 2014; 16: 87–95.

Ahre´n B and Holst JJ. The cephalic insulin response to meal ingestion in humans is dependent on both cholinergic and noncholinergic mechanism and is important for postprandial glycaemia. Diabetes. 2001; 50:1030–1038.

Straub SG and Sharp GWG. Glucose-stimulated signaling pathways in biphasic insulin secretion. Diabetes Metab Res Rev. 2002; 18:451–463.

Nesher R and Cerasi E. Modelling phasic insulin release: immediate and time-dependent effects of glucose. Diabetes. 2002; 51(Suppl 1):S53–59.

Gordon CW and Susan BW. Five stages of evolving B-Cell dysfunction during progression to diabetes. Diabetes. 2004; 53 (Suppl. 3):S16 –210.

Diabetes trial unit. The Oxford centre for Diabetes, Endocrinology and Metabolism, University of Oxford available from https://www.dtu.ox.ac.uk/homacalculator/2004.

Arslanian SA, Bacha F, Saad R and Gungor N. Family history of type 2 diabetes is associated with decreased insulin sensitivity and an impaired balance between insulin sensitivity and insulin secretion in white youth. Diabetes Care. 2005; 28:115-119.

Flores JC, Hirschhorn J and Altshuler D. The inherited basis of diabetes mellitus: implications for the genetic analysis of complex traits. Annu Rev Genomics Hum Genet, 2003. 4: 257-291.

Gloyn AL. The search for type 2 diabetes genes. Ageing Res Rev, 2003. 2: 111-127.

Hansen L. Candidate genes and late-onset type 2 diabetes mellitus. Susceptibility genes or common polymorphisms? Dan Med Bull. 2003. 50: 320-346.

DeFronzo RA. Pathogenesis of type 2 diabetes mellitus. Med Clin N Am. 2004; 88 ; 787–835.

Jin OC, Dong HC, Dong JC and Min YC. Associations among Body Mass Index, Insulin Resistance, and Pancreatic ß-Cell Function in Korean Patients with New-Onset Type 2 Diabetes. Korean J Intern Med. 2012; 27: 66-71.

Kasuga M. Insulin resistance and pancreatic B-cell failure. The Journal of Clinical Investigation. 2006, 116; 7: 1756-1760.

Weyer C, Hanson RL, Tataranni PA, Bogardus C and Pratley RE. A high fasting plasma insulin concentration predicts type 2 diabetes independent of insulin resistance. Evidence for a pathogenic role of relative hyperinsulinaemia. Diabetes. 2000; 49: 2094–2101.

Rahim M, Qureshi MA, Sharafat S et al. Lipid Profile and Growth Indicators among Offspring’s of Diabetic Parents in Karachi, Pakistan. J Diabetes Metab. 2014; 5: 443-448.

Zafar U, Asrar A and Gohar B. Anthropometric Parameters of Central Obesity in Non-Diabetic Offspring of Type 2 Diabetics and non-diabetic offspring of non-diabetics. Pak J Med Health Sci. 2015. 9; 3: 801-803.

Adeleye J.O and Abbiyesuku F.M. Anthropometric characteristics of offsprings of Nigerian Type 2 diabetics. Nigerian Journal of Clinical Practice 2002; 5 (2); 75-80.

Arslanian S and Suprasongsin C. Insulin sensitivity, lipids, and body composition in childhood: is “syndrome X” present? J Clin Endocrinol Metab. 1996; 81: 1058–1062.

Caprio S, Bronson M, Sherwin RS, et al. Co-existence of severe insulin resistance and hyperinsulinaemia in pre-adolescent obese children. Diabetologia. 1996; 39:1489–1497.