Diabetes & metabolic syndrome · 2018
Is there a relationship between stature and age of onset of type 2 Diabetes?
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Gloria-Bottini F, Antonacci E, Neri A, Magrini A, Bottini E
Аннотация
AIMS: MSP1A and MSP1B polymorphic sites located in the GH genomic area have been found associated with GH response to insulin stimulation, with familiar short stature and with age at onset of Type 2 Diabetes (T2D). These observations prompted us to search for a possible relationship between stature and age at onset of the disease.
METHODS: We have reexamined the data of 272 subjects with T2D mellitus.
RESULTS: There is a highly significant negative correlation between stature and age at onset in non obese females (p < 0.001) but not in obese females and in males. In non obese females with stature within the first quartile the mean age at onset is 62 years while in those with a stature greater than the first quartlile the mean age at onset is 52 yesrs (p < 0.001). No difference is observed in obese females and males.
CONCLUSIONS: These observations suggest the existence of different mechanisms underlying susceptibility to T2D. In addition to the well known increased risk due to obesity, endocrine dysfunctions related to genetic variability within the GH genomic area could represent another mechanism operating in non obese females. A cluster of non obese women characterized by short stature and late onset of diabetes seems to be separated by this mechanism from other women.
METHODS: We have reexamined the data of 272 subjects with T2D mellitus.
RESULTS: There is a highly significant negative correlation between stature and age at onset in non obese females (p < 0.001) but not in obese females and in males. In non obese females with stature within the first quartile the mean age at onset is 62 years while in those with a stature greater than the first quartlile the mean age at onset is 52 yesrs (p < 0.001). No difference is observed in obese females and males.
CONCLUSIONS: These observations suggest the existence of different mechanisms underlying susceptibility to T2D. In addition to the well known increased risk due to obesity, endocrine dysfunctions related to genetic variability within the GH genomic area could represent another mechanism operating in non obese females. A cluster of non obese women characterized by short stature and late onset of diabetes seems to be separated by this mechanism from other women.