Incretin effect and glucagon responses to oral and intravenous glucose in patients with maturity-onset diabetes of the young-type 2 and type 3

Diabetes

Volumn 63, Issue 8, 2014, Pages 2838-2844

  Østoft, Signe H ^a,b,c   Bagger, Jonatan I ^a,b,c   Hansen, Torben ^c,d   Pedersen, Oluf ^c   Holst, Jens J ^b,c   Knop, Filip K ^a,b,c   Vilsbøll, Tina ^a  

^a GENTOFTE UNIVERSITY HOSPITAL   (Denmark)

^b UNIVERSITY OF COPENHAGEN   (Denmark)

^c Capital Region   (Denmark)

^d UNIVERSITY OF SOUTHERN DENMARK   (Denmark)

Author keywords

[No Author keywords available]

Indexed keywords

ADMINISTRATION, INTRAVENOUS; ADMINISTRATION, ORAL; ADULT; DIABETES MELLITUS, TYPE 2; FEMALE; GASTRIC EMPTYING; GASTRIC INHIBITORY POLYPEPTIDE; GENE EXPRESSION REGULATION; GLUCAGON; GLUCAGON-LIKE PEPTIDE 1; GLUCOKINASE; GLUCOSE; HEPATOCYTE NUCLEAR FACTOR 1-ALPHA; HUMANS; INCRETINS; INSULIN RESISTANCE; MALE; MIDDLE AGED;

EID: 84903517797     PISSN: 00121797     EISSN: 1939327X     Source Type: Journal    
DOI: 10.2337/db13-1878     Document Type: Article

References (24)

1. Andersen G, Hansen T, Pedersen O. Genetics of common forms of gly-caemia with pathological impact on vascular biology: are we on the right track? Curr Mol Med 2005; 5:261-274
2. Hattersley A, Bruining J, Shield J., Njolstad P, Donaghue K; International Society for Pediatric and Adolescent Diabetes. ISPAD Clinical Practice Consensus Guidelines 2006-2007. The diagnosis and management of monogenic diabetes in children. Pediatr Diabetes 2006; 7:352-360
3. Murphy R, Ellard S, Hattersley AT Clinical implications of a molecular genetic classification of monogenic beta-cell diabetes. Nat Clin Pract Endocrinol Metab 2008; 4:200-213
4. Johansen A, Ek J, Mortensen H.B., Pedersen O., Hansen T. Half of clinically defined maturity-onset diabetes of the young patients in Denmark do not have mutations in HNF4A, GCK, and TCF1. J Clin Endocrinol Metab 2005; 90:4607-4614
5. McCarthy MI, Hattersley AT Learning from molecular genetics: novel insights arising from the definition of genes for monogenic and type 2 diabetes. Diabetes 2008; 57:2889-2898
6. Pearson ER, Starkey BJ, Powell R.J., Gribble FM, Clark PM, Hattersley AT. Genetic cause of hyperglycaemia and response to treatment in diabetes. Lancet 2003; 362:1275-1281
7. Byrne MM, Sturis J, Clément K, et al. Insulin secretory abnormalities in subjects with hyperglycemia due to glucokinase mutations. J Clin Invest 1994; 93:1120-1130
8. Creutzfeldt W, Nauck M. Gut hormones and diabetes mellitus. Diabetes Metab Rev 1992; 8:149-177
9. Verbeke G, Molenberghs G. Linear Mixed Models for Longitudinal Data. New York, Springer, 2000, p. 580
10. Pearson ER, Velho G, Clark P., et al. beta-cell genes and diabetes: quantitative and qualitative differences in the pathophysiology of hepatic nuclear factor-1alpha and glucokinase mutations. Diabetes 2001; 50(Suppl. 1):S101-S107
11. Pontoglio M, Sreenan S, Roe M., et al. Defective insulin secretion in hepa-tocyte nuclear factor 1alpha-deficient mice. J Clin Invest 1998; 101:2215-2222
12. Wang H, Maechler P, Hagenfeldt K.A., Wollheim CB. Dominant-negative suppression of HNF-1alpha function results in defective insulin gene transcription and impaired metabolism-secretion coupling in a pancreatic beta-cell line. EMBO J 1998; 17:6701-6713
13. Wollheim CB. Beta-cell mitochondria in the regulation of insulin secretion: a new culprit in type II diabetes. Diabetologia 2000; 43:265-277
14. Tripathy D, Carlsson AL, Lehto M, Isomaa B., Tuomi T, Groop L. Insulin secretion and insulin sensitivity in diabetic subgroups: studies in the prediabetic and diabetic state. Diabetologia 2000; 43:1476-1483
15. Vaxillaire M, Pueyo ME, Clément K, et al. Insulin secretion and insulin sensitivity in diabetic and non-diabetic subjects with hepatic nuclear factor-1alpha (maturity-onset diabetes of the young-3) mutations. Eur J Endocrinol 1999; 141:609-618
16. Murphy R, Tura A, Clark P.M., Holst JJ, Mari A, Hattersley AT. Glucokinase, the pancreatic glucose sensor, is not the gut glucose sensor. Diabetologia 2009; 52:154-159
17. Ekholm E, Shaat N, Holst JJ Characterization of beta cell and incretin function in patients with MODY1 (HNF4A MODY) and MODY3 (HNF1A MODY) in a Swedish patient collection. Acta Diabetol 2012; 49:349-354
18. Vilsbøll T., Knop FK, Krarup T, et al The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide-regardless of etiology and phenotype. J Clin Endocrinol Metab 2003; 88:4897-4903
19. Thorens B. Expression cloning of the pancreatic beta cell receptor for the gluco-incretin hormone glucagon-like peptide 1. Proc Natl Acad Sci U S A 1992; 89:8641-8645
20. Gromada J, Ding WG, Barg S, Renström E, Rorsman P. Multisite regulation of insulin secretion by cAMP-increasing agonists: evidence that glucagon-like peptide 1 and glucagon act via distinct receptors. Pflugers Arch 1997; 434:515-524
21. Meier JJ, Nauck MA Is the diminished incretin effect in type 2 diabetes just an epi-phenomenon of impaired beta-cell function? Diabetes 2010; 59:1117-1125
22. Knop FK, Vilsbøll T, Madsbad S., Holst JJ, Krarup T. Inappropriate suppression of glucagon during OGTT but not during isoglycaemic i.v. glucose infusion contributes to the reduced incretin effect in type 2 diabetes mellitus. Diabetologia 2007; 50:797-805
23. Katra B, Klupa T, Skupien J., et al. Dipeptidyl peptidase-IV inhibitors are efficient adjunct therapy in HNF1A maturity-onset diabetes of the young patients-report of two cases. Diabetes Technol Ther 2010; 12:313-316
24. Docena MK, Faiman C, Stanley C.M., Pantalone KM. MODY-3: novel HNF1A mutation and the utility of glucagon-like peptide (GLP)-1 receptor agonist therapy. Endocr Pract 2013; 6:1-14