Association between infant growth before onset of juvenile type-1 diabetes and autoantibodies to IA-2

Bruining, G. J.

doi:10.1016/s0140-6736(00)02612-x

Cited by 86 publications

(81 citation statements)

References 4 publications

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“…Increased height and linear growth in childhood have been reported to be a risk factor for diabetes [17][18][19]. In the present study we failed to confirm an increased height based on SDS in children developing diabetes.…”

Section: Discussioncontrasting

confidence: 87%

“…Retrospective studies of children with diabetes have reported increased linear growth up to 7 years before onset of disease [17] as well as increased height and weight standard deviation scores (SDS) from 1 month of age [18] and increased growth in length between 1 and 3 years of age [19,20]. The authors of the latter study corrected growth for mid-parental height (MPH), which is known to correlate with both birthweight and birth length [21], and with postnatal growth of the child [21,22].…”

Section: Introductionmentioning

confidence: 99%

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Children developing type 1 diabetes before 6 years of age have increased linear growth independent of HLA genotypes

et al. 2008

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Aims/hypothesis High birthweight and increased childhood growth are risk factors for type 1 diabetes. Relative birthweight is associated with HLA genotypes that confer a high risk of diabetes. Our aims were to test whether young children prior to clinical onset of type 1 diabetes have increased: (1) birthweight or birth length standard deviation scores (SDS); (2) height development SDS; or (3) BMI SDS during first 18 months of life and whether these parameters are related to HLA genotypes or mid-parental height (MPH). Methods Birthweight, birth length, weight and height were obtained from 58 type 1 diabetes children and 155 controls matched for HLA or not in the Diabetes Prediction in Skåne study. Results Birth length SDS corrected for MPH was increased in children developing diabetes compared with all (p< 0.048) and with non-HLA-(p<0.050) but not with HLAmatched controls. Children developing diabetes had increased height gain at 0 to 18 months of age (p<0.005). Diabetic children were significantly taller from 6 to 18 months of age when correcting for MPH compared with non-HLA-matched as well as HLA-matched controls, but BMI was not increased. Conclusions/interpretation Birth length SDS was associated with diabetes risk HLA. When corrected for MPH, children developing diabetes were taller at birth than non-HLA-but not taller than HLA-matched controls. Diabetic children had increased MPH-corrected height up to 18 months of age compared with both HLA-and non-HLA-matched controls. High-risk HLA affects prenatal growth, but other factors may explain the increased postnatal linear growth in children developing diabetes.

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Section: Discussioncontrasting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Children developing type 1 diabetes before 6 years of age have increased linear growth independent of HLA genotypes

et al. 2008

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“…Vitamin D-deficient NOD mice are lighter and smaller at 15 days of age but they reach the same weight as control mice around weaning at 30 days of age. This lower weight during the first days of life, probably due to the vitamin D deficiency of the dams, followed by a more rapid weight gain in the weeks thereafter might be another factor contributing to the diabetes presentation since also in humans, rapid growth and weight gain are implicated in Type 1 diabetes acceleration through increased metabolic demand [39,40,41].…”

Section: Discussionmentioning

confidence: 99%

Vitamin D deficiency in early life accelerates Type 1 diabetes in non-obese diabetic mice

et al. 2004

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Aims/hypothesis. 1,25-dihydroxyvitamin D 3 , the active form of vitamin D, prevents Type 1 diabetes in non-obese diabetic (NOD) mice. Epidemiological data show a threefold increase in human Type 1 diabetes when vitamin D deficiency was present in the first months of life. To evaluate whether a similar dietary deficiency affects diabetes incidence in NOD mice, we generated NOD mice with vitamin D deficiency in early life. Methods. Breeding pairs of NOD mice, as well as their offspring (test mice), were kept in surroundings devoid of ultraviolet light and were fed a vitamin Ddepleted diet for 100 days. Mice were followed for 250 days. Results. At 250 days, 35% (12/35) male and 66% (22/33) female vitamin D-deficient mice were diabetic compared to 15% (6/40, p=0.05) and 45% (13/29, p<0.01) of the control mice. At 100 days no difference in insulitis was seen, but more vitamin D-deficient mice were glucose intolerant. Higher IL1 expression was detected in islets of vitamin D-deficient mice and their peritoneal macrophages had an aberrant cytokine profile (low IL1 and IL6, high IL15). Thymus and lymph nodes of vitamin D-deficient mice contained less CD4 + CD62L + cells. Conclusion/interpretation. Vitamin D status increases the expression of Type 1 diabetes in NOD mice. Our data in NOD mice, as well as human epidemiological data, point to the importance of preventing vitamin D deficiency in early childhood. Controlling this dietary factor could be an easy and safe way to reduce the incidence of Type 1 diabetes in subjects who are genetically at risk. [Diabetologia (2004)

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“…We have previously shown an association of birth weight, infant growth and autoantibodies against IA-2 with increased risk to develop Type 1 diabetes [67]. It is unclear to what extent this predisposition is determined by endogenous (genetic) or exogenous factors.…”

Section: Genetic and Environmental Factors Associated With T-cell Autmentioning

confidence: 99%

The role of T-cells in the pathogenesis of Type 1 diabetes: From cause to cure

2003

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Association between infant growth before onset of juvenile type-1 diabetes and autoantibodies to IA-2

Cited by 86 publications

References 4 publications

Children developing type 1 diabetes before 6 years of age have increased linear growth independent of HLA genotypes

Children developing type 1 diabetes before 6 years of age have increased linear growth independent of HLA genotypes

Vitamin D deficiency in early life accelerates Type 1 diabetes in non-obese diabetic mice

The role of T-cells in the pathogenesis of Type 1 diabetes: From cause to cure

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