Age, body mass index and Type 2 diabetes?associations modified by ethnicity

Group, The DECODE-DECODA Study

doi:10.1007/s00125-003-1158-9

Cited by 172 publications

(42 citation statements)

References 41 publications

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“…With 53% of the cases presenting with osmotic symptoms including weight loss, the BMI recorded at diagnosis may be lower than earlier in the disease process. Asian children present with Type 2 diabetes at a significantly lower BMI than do white children, which has been described previously 21 and may be related to ethnic differences in visceral fat distribution which corresponds to increased metabolic risk. Obesity prevalence in the UK has increased dramatically over the last 20 years.…”

Section: Discussionsupporting

confidence: 55%

Continuing rise of Type 2 diabetes incidence in children and young people in the UK

et al. 2018

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AimsTo estimate the incidence of Type 2 diabetes in children aged <17 years, compare this with similar data 10 years ago, and characterize clinical features at diagnosis in the UK and Republic of Ireland.MethodsUsing the British Paediatric Surveillance Unit reporting framework, cases of Type 2 diabetes diagnosed in children aged <17 years between 1 April 2015 and 30 April 2016 were reported each month.ResultsA total of 106 cases were reported, giving a UK incidence of 0.72/100 000 (95% CI 0.58–0.88). Children from ethnic minorities had significantly higher incidence compared with white children (0.44/100 000) with rates of 2.92/100 000 and 1.67/100 000, in Asian and BACBB (black/African/Caribbean/black British) children respectively. Sixty‐seven percent were girls and 81% had a family history of Type 2 diabetes. The mean BMI sd score at diagnosis was 2.89 (2.88, girls; 2.92, boys); 81% were obese. Children of Asian ethnicity had a significantly lower BMI sd score compared with white children (P<0.001). There was a trend in increased incidence from 2005 to 2015, with a rate ratio of 1.35 (95% CI 0.99–1.84), although this was not statistically significant (P=0.062). There was statistical evidence of increased incidence among girls (P=0.03) and children of South‐Asian ethnicity (P=0.01) when comparing the 2005 and 2015 surveys.ConclusionsType 2 diabetes remains far less common than Type 1 diabetes in childhood in the UK, but the number of cases continues to rise, with significantly increased incidence among girls and South‐Asian children over a decade. Female gender, family history, non‐white ethnicity and obesity were found to be strongly associated with the condition.

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Section: Discussionsupporting

confidence: 55%

Continuing rise of Type 2 diabetes incidence in children and young people in the UK

et al. 2018

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“…These findings can explain the existence of ‘benign’ and ‘malign’ obesity wherein insulin resistance is not observed in all individuals with high BMIs. They may also explain the very high incidence of insulin resistance and diabetes in ethnic populations that display relatively low BMIs associated with high waist circumferences or waist-to-hip ratios, reflecting elevated visceral obesity [6]. …”

Section: Not All Forms Of Obesity Results In Insulin Resistancementioning

confidence: 99%

What causes the insulin resistance underlying obesity?

Hardy

Czech

Corvera

2012

Current Opinion in Endocrinology, Diabetes &Amp; Obesity

416

305

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Purpose of review The association between obesity and insulin resistance is an area of much interest and enormous public health impact, with hundreds of articles being published in the last year focused on the possible mechanisms that underlie this association. The purpose to this review is to highlight some of the key recent literature with emphasis on emerging concepts. Recent findings The specific link between visceral adipose tissue accumulation and insulin resistance continues to be discerned. Visceral adiposity is correlated with accumulation of excess lipid in liver, and results in cell autonomous impairment in insulin signaling. Visceral adipose tissue is also prone to inflammation and inflammatory cytokine production, which also contribute to impairment in insulin signaling. The expansion of visceral adipose tissue and excess lipid accumulation in liver and muscle may result from limited expandability of subcutaneous adipose tissue, due to the properties of its extracellular matrix and capacity for capillary growth. Summary Recent studies underscore the need to better understand the mechanisms linking visceral adiposity with liver fat accumulation, the mechanisms by which ectopic fat accumulation cause insulin resistance, and the mechanisms by which the size of adipose tissue depots is determined.

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“…Nevertheless, there is evidence in the literature showing gender differences in the vascular alterations in diabetes mellitus. Diabetes has been shown to be a stronger risk factor for coronary disease [13] and cerebrovascular complications [14] in women than in men, whereas diabetic women showed a higher risk for death from cardiovascular disease than diabetic men [15]. Diabetes reduces the relaxation to acetylcholine and iloprost only in diabetic female rats [16].…”

Section: Introductionmentioning

confidence: 99%

Correction of Endothelial Dysfunction in Diabetic Female Rats by Tetrahydrobiopterin and Chronic Insulin

Akamine

Kawamoto²,

Scavone³

et al. 2006

J Vasc Res

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Diabetes-induced vascular dysfunction has mainly been studied in males. However, the mechanisms involved may not correspond to those in females. Here we analyzed the effects of tetrahydrobiopterin (BH₄) and chronic insulin on the physiology of mesenteric arterioles of alloxan-diabetic female rats. The parameters studied were the mesenteric arteriolar reactivity (intravital microscopy), nitric oxide synthase (NOS) activity (conversion of L-arginine to L-citrulline), eNOS gene expression (RT-PCR), NO production (diaminofluorescein), reactive oxygen species (ROS) generation (intravital fluorescence microscopy) and Cu/Zn superoxide dismutase (SOD) activity (spectrophotometry) and gene expression (RT-PCR). The reduced endothelium-dependent vasodilation of diabetic females was corrected by both BH₄ and insulin. NOS activity was decreased by diabetes, but insulin did not correct it. However, NOS expression was not modified by either diabetes or insulin. Arterioles of diabetic rats exhibited lower NO production, which was fully corrected by BH₄ and only partially by insulin. ROS generation was increased in diabetic rats, and both BH₄ and insulin normalized it. Diabetes did not change SOD activity and gene expression. However, insulin increased SOD activity but not its expression. Our data suggest that, similarly to males, endothelial dysfunction in female diabetic rats involves an altered ROS/NO imbalance. In contrast to males, however, insulin does not regulate NOS in the microcirculation of diabetic females.

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Age, body mass index and Type 2 diabetes?associations modified by ethnicity

Cited by 172 publications

References 41 publications

Continuing rise of Type 2 diabetes incidence in children and young people in the UK

Continuing rise of Type 2 diabetes incidence in children and young people in the UK

What causes the insulin resistance underlying obesity?

Correction of Endothelial Dysfunction in Diabetic Female Rats by Tetrahydrobiopterin and Chronic Insulin

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