Youth Type 2 Diabetes

Güngör, Neslihan; Bacha, Fida; Saad, Rola; Janosky, Janine E.; Arslanian, Silva

doi:10.2337/diacare.28.3.638

Cited by 152 publications

(150 citation statements)

References 32 publications

Supporting

Mentioning

122

Contrasting

Unclassified

Order By: Relevance

“…Second-phase insulin is ϳ60% lower in type 2 diabetes than in NGT, but it is preserved in IGT. This is consistent with our previous report of decreased second-phase insulin levels in type 2 diabetic subjects vs. obese control subjects (23) and with the findings of Weiss et al (20) of decreased glucose sensitivity of secondphase insulin in type 2 diabetic subjects.…”

Section: Clamp Datasupporting

confidence: 83%

“…This is consistent with our previous report of increased HGP in type 2 diabetic youth than in obese control subjects (23) and with adult data suggesting that increased endogenous glucose production contributes to fasting hyperglycemia (17). Finally, our data demonstrate that firstphase insulin and GDI are significant determinants of measures of glycemic regulation, including fasting glucose and 2-h glucose during the OGTT.…”

Section: Clamp Datasupporting

confidence: 82%

“…However, data analysis performed separately in the type 2 diabetic subjects did not show any significant differences in A1C or GDI in the four treatment groups. Also, the majority of these adolescents (12 out of 17) were studied within 6 months of diagnosis of type 2 diabetes, with no significant difference in GDI or A1C when evaluated according to duration of diabetes and no relationship between duration of diabetes and A1C, which was consistent with our previous findings (23). The other limitation of the relatively smaller sample size (NGT ϭ 12) is offset by the use of the clamp methodology, which allowed us to demonstrate significant differences among the three groups.…”

Section: Clamp Datasupporting

confidence: 82%

See 2 more Smart Citations

In Vivo Insulin Sensitivity and Secretion in Obese Youth

Bacha

Güngör²,

Lee³

et al. 2009

Diabetes Care

Self Cite

131

View full text Add to dashboard Cite

OBJECTIVE -Impaired glucose tolerance (IGT) represents a pre-diabetic state. Controversy continues in regards to its pathophysiology. The aim of this study was to investigate the differences in insulin sensitivity (IS) and secretion in obese adolescents with IGT compared with those with normal glucose tolerance (NGT) and type 2 diabetes.RESEARCH DESIGN AND METHODS -A total of 12 obese adolescents with NGT, 19 with IGT, and 17 with type 2 diabetes underwent evaluation of insulin sensitivity (3-h hyperinsulinemic [80mu/m 2 /min]-euglycemic clamp), first-phase insulin and second-phase insulin secretion (2-h hyperglycemic clamp), body composition, and abdominal adiposity. Glucose disposition index (GDI) was calculated as the product of first-phase insulin ϫ insulin sensitivity.RESULTS -Insulin-stimulated glucose disposal was significantly lower in subjects with type 2 diabetes compared with subjects with NGT and IGT, with no difference between the latter two. However, compared with youth with NGT, youth with IGT have significantly lower first-phase insulin and C-peptide levels and GDI (P ϭ 0.012), whereas youth with type 2 diabetes have an additional defect in second-phase insulin. Fasting and 2-h glucose correlated with GDI (r ϭ Ϫ0.68, P Ͻ 0.001 and r ϭ Ϫ0.73, P Ͻ 0.001, respectively) and first-phase insulin but not with insulin sensitivity.CONCLUSIONS -Compared with youth with NGT, obese adolescents with IGT have evidence of a ␤-cell defect manifested in impaired first-phase insulin secretion, with a more profound defect in type 2 diabetes involving both first-and second-phase insulin. GDI shows a significantly declining pattern: it is highest in NGT, intermediate in IGT, and lowest in type 2 diabetes. Such data suggest that measures to prevent progression or conversion from prediabetes to type 2 diabetes should target improvement in ␤-cell function.

show abstract

Section: Clamp Datasupporting

confidence: 83%

Section: Clamp Datasupporting

confidence: 82%

Section: Clamp Datasupporting

confidence: 82%

See 1 more Smart Citation

In Vivo Insulin Sensitivity and Secretion in Obese Youth

Bacha

Güngör²,

Lee³

et al. 2009

Diabetes Care

Self Cite

131

View full text Add to dashboard Cite

show abstract

“…Секреция оставалась высокой только на протя-жении первых 3 лет от диагностики заболевания, в дальнейшем происходило ее значимое снижение. Имеются данные, что у молодежи с СД2 снижение функции β-клеток происходит быстрее, чем у взрос-лых, примерно на 15% в год [19]. В исследованиях, где диагностика СД2 была основана только на соче-тании СД с синдромом ИР и высоким уровнем ин-сулина в дебюте заболевания, отмечено еще более быстрое снижение секреторной активности β-клеток с достижением абсолютного дефицита уже в первые 1-3 года, что свидетельствует, по нашему мнению, о наличии у части пациентов СД1 в сочета-нии с ожирением.…”

Section: Discussionunclassified

Clinical polymorphism of type 2 diabetes in children — the first study in Russia

Еремина¹,

Кураева²,

Зильберман³

et al. 2015

Probl Endokrinol (Mosk)

View full text Add to dashboard Cite

1 ФГБУ «Эндокринологический научный центр» Минздрава России, Москва; 2 ГБОУ ВПО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России Цель -изучить особенности диагностики, клинических проявлений и течения сахарного диабета 2-го типа (СД2) у детей в Российской популяции. Материал и методы. Обследованы 80 детей с СД2, из них 70 -в динамике, длительность наблюдения -2,6 года (1,5; 4,5). Кроме общеклинического обследования, определяли секрецию инсулина, HLA-полиморфизм DQ и DR-генов, специ-фические для сахарного диабета 1-го типа (СД1) аутоантитела (Ат). Результаты. Медиана возраста диагностики СД2 -13 лет (11,5; 15,5 года). Наследственность по СД2 отягощена у 58,8% детей. Только 26,3% детей с СД2 предъявляли классические для СД жалобы. У 65% СД2 диагностирован при обследо-вании по поводу ожирения (у 51,9% из них при проведении перорального глюкозотолерантного теста (ПГТТ), у 48,1% -гликемия натощак превышала 7,0 ммоль/л). Кетонурия в дебюте заболевания отмечалась у 21,3%; 85% имели ожире-ние или избыточную массу тела. Ат (ICA и IAA) выявлялись в 15,2% случаев, причем в невысоком титре. HLA-генотипы высокого риска СД1 выявлены в 5,5% случаев. Уровень гликрованного гемоглобина в дебюте заболевания -7,1% (6,3; 8,5%), в первые 3 года у большинства детей его уровень был ниже 6,5%. Секреция инсулина и С-пептида в первые 3 года сохранялась на высоком уровне, у 81,3% детей в дебюте отмечалась инсулинорезистентность, при динамическом наблюдении ее частота значимо не менялась. Инсулинотерапия в начальном периоде заболевания была назначена 30% пациентов. Через 3 года лишь 8% детей получали инсулин при сохранной собственной секреции гормона. Выводы. Бессимптомное начало заболевания требует активной диагностики СД2 в группах высокого риска: при наличии ожирения, отягощенной по СД2 наследственности, в пубертатный период. У 1 / 3 детей СД2 диагностируется только при использовании ПГТТ. Для СД2 у детей и подростков характерен клинический полиморфизм в виде острой манифестации в 21% случаев, отсутствия ожирения в 15%, отсутствия инсулинорезистентности в 18%, что требует дифференциальной диагностики этих случаев с СД1 и MODY. При СД2 в детском возрасте на протяжении 3 лет сохраняется высокий уровень инсулина и С-пептида и отсутствует потребность в инсулинотерапии. При этом наличие ICA и IAA в невысоком титре не противоречит диагнозу СД2. Objective. To elucidate the specific features of diagnostics, clinical course and manifestations of type 2 diabetes mellitus (DM2) in the children of the Russian population. Material and methods. A total of 80 children presenting with DM2 were enrolled in the study including 70 available for the dynamic examination, with the follow-up period of 2.6 years (1.5; 4.5). The general clinical examination of the patients was supplemented by measuring insulin secretion, studying HLA-polymorphism of the DQ and DR-genes, and determination of type 1 diabetes (DM1) -related specific antibodies (At). Results. The median age at diagnosis of DM2 was 13 years (11.5; 15.5). ...

show abstract

“…The deterioration of glucose tolerance is accompanied by a severe degree of insulin resistance [5,6].…”

mentioning

confidence: 99%

Insulin Resistance, the Metabolic Syndrome and Type 2 Diabetes

Lévy-Marchal¹

2006

Yearbook of Pediatric Endocrinology 2006

View full text Add to dashboard Cite

Experimental studies on the mechanisms of insulin resistance are exciting this year. Just look at the physiology of PPAR-␦ and the newly described functions of insulin and also vaspin coming on the market! There is not a single month without a new hormone or a new function of the adipose tissue being brought to light. Progress made over the past few months on the understanding of insulin resistance itself and on the pathology and the connections between fat, muscle, liver and ␤-cell are just incredible. Mirroring these breakthroughs and supported by the increasing and alarming extension of obesity, numerous clinical studies are related to risk factors for insulin resistance and the metabolic syndrome in childhood. The selection of publications is sometimes critical and here we try to focus on specific and pediatric aspects of the debate 'whether the metabolic syndrome is for real', pointing to important subjects relevant to clinical practice. Mechanism of the year Antagonistic actions of ecdysone and insulins determine final size in DrosophilaColombani J, Bianchini L, Layalle S, Pondeville E, Dauphin-Villemant C, Antoniewski C, Carre C, Noselli S, Leopold P CNRS/University of Nice-Sophia Antipolis, UMR6543, Nice, France Science 2005;310:667-670 Background: All animals coordinate growth and maturation to reach their final size and shape. In insects, insulin family molecules control growth and metabolism, whereas pulses of the steroid 20-hydroxyecdysone initiate major developmental transitions. Methods: Construction of a genetic model for modulation of the concentrations of ecdysone. Results: The authors show that 20-hydroxyecdysone signaling also negatively controls animal growth rates by impeding general insulin signaling involving localization of the transcription factor dFOXO and transcription of the translation inhibitor 4E-BP. The authors also demonstrate that the larval fat body, equivalent to the vertebrate liver, is a key relay element for ecdysone-dependent growth inhibition. Conclusion: Ecdysone counteracts the growth-promoting action of insulin, thus forming a humoral regulatory loop that determines organismal size.This experimental work dissects the mechanisms of growth of the larva of the Drosophila with opposite actions of steroids and insulin/IGFs. The observations reveal a key role of the fat body of the larva, integrating nutritional inputs and controlling the insulin-signaling pathway to modulate organismal growth. This is an additional and fascinating example of interferences of nutrition, metabolism (and insulin) and growth. How, then, is growth connected to developmental timing? These findings place this hormone in a central position for coordinating these two key processes and controlling organismal size. 164Claire Levy-Marchal Clin Endocrinol Metab 2006;91:401-404 Background: Type 2 diabetes (T2D) in obese children is an emerging problem, including in Europe. Its presentation at diagnosis very often differs from that in adults. Aim: The objective of this study was to investigate th...

show abstract

Youth Type 2 Diabetes

Cited by 152 publications

References 32 publications

In Vivo Insulin Sensitivity and Secretion in Obese Youth

In Vivo Insulin Sensitivity and Secretion in Obese Youth

Clinical polymorphism of type 2 diabetes in children — the first study in Russia

Insulin Resistance, the Metabolic Syndrome and Type 2 Diabetes

Contact Info

Product

Resources

About