Literature DB >> 32064729

Beta cell function and insulin sensitivity in obese youth with maturity onset diabetes of youth mutations vs type 2 diabetes in TODAY: Longitudinal observations and glycemic failure.

Silva Arslanian1, Laure El Ghormli2, Morey H Haymond3, Christine L Chan4, Steven D Chernausek5, Rachelle G Gandica6, Rose Gubitosi-Klug7, Lynne L Levitsky8, Maggie Siska9, Steven M Willi10.   

Abstract

OBJECTIVE: In treatment options for type 2 diabetes in adolescents and youth (TODAY), 4.5% of obese youth clinically diagnosed with type 2 diabetes (T2D) had genetic variants consistent with maturity onset diabetes of youth (MODY) diagnosis. The course of IS and β-cell function in obese youth with MODY remains unknown. In this secondary analysis, we examined IS and β-cell function in MODY vs. non-MODY obese youth at randomization and over time.
METHODS: Genetic data in TODAY included 426 non-MODY (T2D) and 22 MODY youth (7 glucokinase MODY mutation positive [GCK-MODY], 12 hepatocyte nuclear factor MODY mutation positive [HNF-MODY], 2 Insulin gene mutation [insulin (INS)-MODY], and 1 Kruppel-like factor 11 [KLF11-MODY]). Oral glucose tolerance test (OGTT)-derived IS, C-peptide index, and β-cell function relative to IS oral disposition index (oDI) was measured at randomization, and over 24 months in addition to total and high-molecular-weight adiponectin (HMWA).
RESULTS: At randomization, IS, total adiponectin, and HMWA were significantly higher in the two MODY groups than in non-MODY. β-cell function measured by C-peptide oDI was 3-fold higher in GCK-MODY than in HNF-MODY and 1.5-fold higher than non-MODY (P for both <.05). Glycemic failure rate was 75.0% in HNF-MODY, 46.9% in non-MODY, and zero in GCK-MODY youth. While the changes in IS and oDI were not different among the three groups in the first 6 months, IS improved from 6 to 24 months in HNF-MODY vs GCK-MODY youth.
CONCLUSIONS: In TODAY, β-cell function at randomization was worse in obese HNF-MODY youth compared with GCK-MODY youth, while insulin sensitivity was worse in non-MODY compared with the other two MODY groups. Over time, IS showed the greatest improvement in HNF-MODY youth. This raises the possibility that TODAY therapeutic modalities of insulin sensitization in these obese HNF-MODY youth may have played a beneficial role.
© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Entities:  

Keywords:  MODY; glycemic control; insulin secretion; insulin sensitivity; type 2 diabetes; youth

Year:  2020        PMID: 32064729      PMCID: PMC7654712          DOI: 10.1111/pedi.12998

Source DB:  PubMed          Journal:  Pediatr Diabetes        ISSN: 1399-543X            Impact factor:   4.866


  49 in total

Review 1.  Maturity-onset diabetes of the young (MODY): an update.

Authors:  Ahmet Anık; Gönül Çatlı; Ayhan Abacı; Ece Böber
Journal:  J Pediatr Endocrinol Metab       Date:  2015-03       Impact factor: 1.634

2.  Characterization of beta cell and incretin function in patients with MODY1 (HNF4A MODY) and MODY3 (HNF1A MODY) in a Swedish patient collection.

Authors:  E Ekholm; N Shaat; J J Holst
Journal:  Acta Diabetol       Date:  2011-07-16       Impact factor: 4.280

3.  Youth type 2 diabetes: insulin resistance, beta-cell failure, or both?

Authors:  Neslihan Gungor; Fida Bacha; Rola Saad; Janine Janosky; Silva Arslanian
Journal:  Diabetes Care       Date:  2005-03       Impact factor: 19.112

4.  Altered insulin secretory responses to glucose in diabetic and nondiabetic subjects with mutations in the diabetes susceptibility gene MODY3 on chromosome 12.

Authors:  M M Byrne; J Sturis; S Menzel; K Yamagata; S S Fajans; M J Dronsfield; S C Bain; A T Hattersley; G Velho; P Froguel; G I Bell; K S Polonsky
Journal:  Diabetes       Date:  1996-11       Impact factor: 9.461

5.  A clinical trial to maintain glycemic control in youth with type 2 diabetes.

Authors:  Phil Zeitler; Kathryn Hirst; Laura Pyle; Barbara Linder; Kenneth Copeland; Silva Arslanian; Leona Cuttler; David M Nathan; Sherida Tollefsen; Denise Wilfley; Francine Kaufman
Journal:  N Engl J Med       Date:  2012-04-29       Impact factor: 91.245

Review 6.  Genetic, metabolic and clinical characteristics of maturity onset diabetes of the young.

Authors:  G Velho; P Froguel
Journal:  Eur J Endocrinol       Date:  1998-03       Impact factor: 6.664

7.  Beta-cell dysfunction, insulin sensitivity, and glycosuria precede diabetes in hepatocyte nuclear factor-1alpha mutation carriers.

Authors:  Amanda Stride; Sian Ellard; Penny Clark; Lynette Shakespeare; Maurice Salzmann; Maggie Shepherd; Andrew T Hattersley
Journal:  Diabetes Care       Date:  2005-07       Impact factor: 19.112

8.  Oral disposition index in obese youth from normal to prediabetes to diabetes: relationship to clamp disposition index.

Authors:  Lindsey George Sjaarda; Fida Bacha; Sojung Lee; Hala Tfayli; Elisa Andreatta; Silva Arslanian
Journal:  J Pediatr       Date:  2012-02-09       Impact factor: 4.406

9.  Primary pancreatic beta-cell secretory defect caused by mutations in glucokinase gene in kindreds of maturity onset diabetes of the young.

Authors:  G Velho; P Froguel; K Clement; M E Pueyo; B Rakotoambinina; H Zouali; P Passa; D Cohen; J J Robert
Journal:  Lancet       Date:  1992-08-22       Impact factor: 79.321

10.  Monogenic diabetes in overweight and obese youth diagnosed with type 2 diabetes: the TODAY clinical trial.

Authors:  Jeffrey W Kleinberger; Kenneth C Copeland; Rachelle G Gandica; Morey W Haymond; Lynne L Levitsky; Barbara Linder; Alan R Shuldiner; Sherida Tollefsen; Neil H White; Toni I Pollin
Journal:  Genet Med       Date:  2017-10-12       Impact factor: 8.822

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  1 in total

Review 1.  Pregnancy in Women With Monogenic Diabetes due to Pathogenic Variants of the Glucokinase Gene: Lessons and Challenges.

Authors:  José Timsit; Cécile Ciangura; Danièle Dubois-Laforgue; Cécile Saint-Martin; Christine Bellanne-Chantelot
Journal:  Front Endocrinol (Lausanne)       Date:  2022-01-05       Impact factor: 5.555

  1 in total

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