Presentation of youth with type 2 diabetes in the Pediatric Diabetes Consortium

Klingensmith, Georgeanna J.; Connor, Crystal G.; Ruedy, Katrina J.; Beck, Roy W.; Kollman, Craig; Haro, Heidi; Wood, Jamie; Lee, Joyce M.; Willi, Steven M.; Cengiz, Eda; Tamborlane, William V.

doi:10.1111/pedi.12281

Cited by 115 publications

(158 citation statements)

References 28 publications

Supporting

Mentioning

129

Contrasting

Unclassified

Order By: Relevance

“…Hence, the stress-enhanced metabolism dysregulation is only amplified in mice exposed to stress during adolescence or younger age. This scenario is supported by recent reports addressing the links between psychological stress and early-onset T2D [48][49][50]. Our mouse model is an appropriate tool to investigate the role of age-dependent stress experience in the pathogenesis of metabolic disorders.…”

Section: Discussionsupporting

confidence: 53%

Stress Aggravates High-Fat-Diet-Induced Insulin Resistance via a Mechanism That Involves the Amygdala and Is Associated with Changes in Neuroplasticity

Tsai

Chen

et al. 2018

Neuroendocrinology

View full text Add to dashboard Cite

Background: The notion that exposure to chronic stress predisposes individuals to developing type 2 diabetes (T2D) has gained much attention in recent decades. Long-term stress induces neuroadaptation in the amygdala and increases corticosterone levels. Corticosterone, the major stress hormone in rodents, induces insulin resistance and obesity in mice. However, little is known about whether the stress-induced amygdalar neuroadaptation could promote the risk of T2D. Methods: We used an 11-week high-fat diet (HFD) feeding paradigm to induce insulin dysfunction in mice, followed by implementation of a 10-day social defeat (SD) stress protocol. Results: Mice receiving SD at the beginning of the HFD feeding aggravated HFD-induced insulin resistance and white adipose tissue expansion. HFD mice had higher levels of plasma corticosterone, which was not affected by the SD. The SD stress upregulated the expression of TrkB and synaptotagmin-4 in the amygdala of HFD mice. Bilateral lesions of the central amygdalae before SD stress inhibited the stress-induced aggravating effect without affecting the HFD-induced elevation of plasma corticosterone. Conclusions: Stress aggravates HFD-induced insulin resistance and neuroadaptation in the amygdala. The HFD-induced insulin resistance is amygdala-dependent. Understanding the role of stress-induced amygdalar adaptation in the development of T2D could inform therapies aimed at reducing chronic stressors to decrease the risk for T2D.

show abstract

Section: Discussionsupporting

confidence: 53%

Stress Aggravates High-Fat-Diet-Induced Insulin Resistance via a Mechanism That Involves the Amygdala and Is Associated with Changes in Neuroplasticity

Tsai

Chen

et al. 2018

Neuroendocrinology

View full text Add to dashboard Cite

show abstract

“…The prevalence of T2DM is highest among racial/ethnic minority youth, whereby approximately 80% of youth with T2DM are from racial/ethnic minority backgrounds [18]. In the treatment options for type 2 diabetes in adolescents and youth (TODAY) study, which had the best characterized cohort of youth with T2DM, 30% of youth were African-American, 40% were Hispanic/Latino, and 6% were American-Indian [3].…”

Section: Racial/ethnic Disparities In Prevalence Glycemic Control Amentioning

confidence: 99%

Social Determinants of Health and Racial/Ethnic Disparities in Type 2 Diabetes in Youth

Butler

2017

Curr Diab Rep

View full text Add to dashboard Cite

Purpose of Review Pervasive disparities in T2DM among minority adults are well-documented, and scholars have recently focused on the role of social determinants of health (SDOH) in disparities. Yet, no research has summarized what is known about racial/ethnic disparities in youth-onset T2DM. This review summarizes the current literature on racial/ethnic disparities in youth-onset T2DM, discusses SDOH that are common among youth with T2DM, and introduces a conceptual model on the possible role of SDOH in youth-onset T2DM disparities. Recent Findings Minority youth have disparities in the onset of T2DM, quality of life, and family burden. Low family income and parental education and high youth stress are common negative SDOH among families of youth with T2DM. No studies have examined the role of SDOH in racial/ethnic disparities in youth-onset T2DM. Summary Future research should examine whether SDOH contribute to disparities in T2DM prevalence and psychosocial outcomes among minority youth.

show abstract

“…First, we cannot rule out the possibility of some misclassification of diabetes type, whereby, in some cases, physicians may have prescribed both insulin and noninsulin antidiabetes medications before making a final diagnosis. Using the data from the Pediatric Diabetes Consortium, Klingensmith et al (31) recently reported that in the initial month after diagnosis of type 2 diabetes around 30% of patients were treated with insulin only. Thus, we may have misclassified a small proportion of type 2 cases as type 1 diabetes or vice versa.…”

Section: Prevalence Of Diabetic Nephropathymentioning

confidence: 99%

Prevalence of Diabetes and Diabetic Nephropathy in a Large U.S. Commercially Insured Pediatric Population, 2002–2013

Jick

Breitenstein

et al. 2015

Diabetes Care

View full text Add to dashboard Cite

OBJECTIVE To estimate the prevalence of diabetes and diabetic nephropathy in a large population of U.S. commercially insured patients aged <18 years from 2002 to 2013. RESEARCH DESIGN AND METHODS Using the U.S. MarketScan Commercial Claims and Encounters Database, we identified 96,171 pediatric patients with diabetes and 3,161 pediatric patients with diabetic nephropathy during 2002–2013. We estimated prevalence of pediatric diabetes overall, by diabetes type, age, and sex, and prevalence of pediatric diabetic nephropathy overall, by age, sex, and diabetes type. RESULTS The annual prevalence of diabetes in the whole pediatric population increased from 1.86 to 2.82 per 1,000 during 2002–2013: 1.48 to 2.32 per 1,000 for type 1 diabetes and 0.38 to 0.67 per 1,000 for type 2 diabetes in 2002–2006 and then 0.56 to 0.49 per 1,000 thereafter. The annual prevalence of diabetic nephropathy in pediatric patients with diabetes increased from 1.16 to 3.44% for all cases and 0.83 to 2.32% for probable cases only in 2002–2013. Prevalence of diabetes and diabetic nephropathy was highest in patients aged 12 to <18 years. While prevalence of type 1 diabetes was higher in male than in female youth, prevalence of type 2 diabetes and diabetic nephropathy was higher in female than in male youth. There was no difference in prevalence of diabetic nephropathy by diabetes type. CONCLUSIONS The prevalence of diabetes and diabetic nephropathy increased in the U.S. MarketScan commercially insured pediatric population from 2002 to 2013. The prevalence of diabetes and diabetic nephropathy markedly increased starting at age 12 years.

show abstract

Presentation of youth with type 2 diabetes in the Pediatric Diabetes Consortium

Cited by 115 publications

References 28 publications

Stress Aggravates High-Fat-Diet-Induced Insulin Resistance via a Mechanism That Involves the Amygdala and Is Associated with Changes in Neuroplasticity

Stress Aggravates High-Fat-Diet-Induced Insulin Resistance via a Mechanism That Involves the Amygdala and Is Associated with Changes in Neuroplasticity

Social Determinants of Health and Racial/Ethnic Disparities in Type 2 Diabetes in Youth

Prevalence of Diabetes and Diabetic Nephropathy in a Large U.S. Commercially Insured Pediatric Population, 2002–2013

Contact Info

Product

Resources

About