Effect of Parental Type 2 Diabetes on Offspring With Type 1 Diabetes (original) (raw)

Influence of childhood parental history of type 2 diabetes on the pre-diabetic and diabetic status in adulthood: the Bogalusa Heart Study

European Journal of Epidemiology, 2009

To assess the association of childhood parental history of type 2 diabetes and the risk of diabetes in adulthood. Observations were made on a community-based cohort of normoglycemic (n = 1619), pre-diabetic (n = 78), and type 2 diabetic (n = 50) adult subjects followed serially for cardiovascular risk factors over 22 years from childhood and noting their relation to a parental history of diabetes. In a longitudinal multivariate model including parental diabetes observed in the offspring's childhood, BMI, MAP, HDL cholesterol, LDL cholesterol, triglycerides, insulin, and glucose, adjusted for age, age 2 , race, sex, and race by sex interaction, parental diabetes and adverse changes in LDL cholesterol and glucose were independently associated with pre-diabetic status in adulthood (regression coefficient [b] = 0.74 (95% CI: 0.04-1.45), 0.44 (95% CI: 0.24-0.64), and 1.99 (95% CI: 1.73-2.25), respectively), while parental diabetes and adverse changes in BMI, HDL cholesterol, and glucose were associated with the diabetic status (b = 1.14 (95% CI: 0.35-1.92), 0.08 (95% CI: 0.05-0.11),-0.51 (95% CI:-1.03 to-0.003), and 1.79 (95% CI: 1.48-2.09), respectively). Childhood parental history of diabetes along with adverse changes in adiposity, glucose, and lipoprotein variables of metabolic syndrome since childhood are associated with the increased risk of pre-diabetic and diabetic status in adulthood. Keywords Cardiovascular risk factor Á Children Á Pre-diabetes Á Type 2 diabetes Á Young adult Á Longitudinal changes Á Parental history of diabetes

Relationship Between Parental Diabetes and Presentation of Metabolic and Glycemic Function in Youth With Type 2 Diabetes: Baseline Findings From the TODAY Trial

Diabetes care, 2015

Children whose parents have diabetes are at increased risk for developing type 2 diabetes. This report assessed relationships between parental diabetes status and baseline demographics, anthropometrics, metabolic measurements, insulin sensitivity, and β-cell function in children recently diagnosed with type 2 diabetes. The sample included 632 youth (aged 10-17 years) diagnosed with type 2 diabetes for <2 years who participated in the TODAY clinical trial. Medical history data were collected at baseline by self-report from parents and family members. Youth baseline measurements included an oral glucose tolerance test and other measures collected by trained study staff. Youth exposed to maternal diabetes during pregnancy (whether the mother was diagnosed with diabetes prior to pregnancy or had gestational diabetes mellitus) were diagnosed at younger ages (by 0.6 years on average), had greater dysglycemia at baseline (HbA1c increased by 0.3% [3.4 mmol/mol]), and had reduced β-cell f...

Original Article OPEN ACCESS Familial early onset of type-2 diabetes mellitus and its complications

Background: Globally, the prevalence of chronic, non-communicable diseases is increasing at an alarming rate. Furthermore, approximately 197 million people worldwide have impaired glucose tolerance. Consequently, diabetes is rapidly emerging as a global health problem that threatens to assume a pandemic level by 2030. In Indian population, genetic predisposition to trigger diabetes at an early age as compared to western counterpart has been focused very much. Aim: To gain further insight into the positive correlation between the diabetes and family history was the objective of this study. Materials and Methods: Patients attending the Diabetes were recruited, diagnosed and analyzed as per WHO criteria. Results: The prevalence of diabetes was higher among patients with diabetic mother (25.6%) compared to patients with diabetic father (21.2%) and there was early onset of type -2 diabetes among patients having both parents with diabetic when compared to other patients. Conclusion: Based on the present observation, it would be appropriate to emphasize again that a strong family history for diabetes, would signal at an early age, the onset of diabetes perhaps with its complications.

Insulin resistance is a poor predictor of type 2 diabetes in individuals with no family history of disease

Proceedings of the National Academy of Sciences, 2003

In normoglycemic offspring of two type 2 diabetic parents, low insulin sensitivity (SI) and low insulin-independent glucose effectiveness (SG) predict the development of diabetes one to two decades later. To determine whether low SI, low SG, or low acute insulin response to glucose are predictive of diabetes in a population at low genetic risk for disease, 181 normoglycemic individuals with no family history of diabetes (FH؊) and 150 normoglycemic offspring of two type 2 diabetic parents (FH؉) underwent i.v. glucose tolerance testing (IVGTT) between the years 1964 -82. During 25 ؎ 6 years follow-up, comprising 2,758 person years, the FH؊ cohort (54 ؎ 9 years) had an age-adjusted incidence rate of type 2 diabetes of 1.8 per 1,000 person years, similar to that in other population-based studies, but significantly lower than 16.7 for the FH؉ cohort. Even when the two study populations were subdivided by initial values of SI and SG derived from IVGTT's performed at study entry, there was a 10-to 20-fold difference in age-adjusted incidence rates for diabetes in the FH؊ vs. FH؉ individuals with low SI and low SG. The acute insulin response to glucose was not predictive of the development of diabetes when considered independently or when assessed as a function of SI, i.e., the glucose disposition index. These data demonstrate that low glucose disposal rates are robustly associated with the development of diabetes in the FH؉ individuals, but insulin resistance per se is not sufficient for the development of diabetes in individuals without family history of disease and strongly suggest a familial factor, not detectable in our current measures of the dynamic responses of glucose or insulin to an IVGTT is an important risk factor for type 2 diabetes. Low SI and low SG , both measures of glucose disposal, interact with this putative familial factor to result in a high risk of type 2 diabetes in the FH؉ individuals, but not in the FH؊ individuals.

Influence of obesity, parental history of diabetes, and genes in type 2 diabetes: A case-control study

Scientific Reports

Obesity, parental history (PH) of type 2 diabetes (T2D), and genes play an important role in T2D development. However, the influence of each factor on T2D variability is unclear. This study aimed to investigate the influence of obesity (body mass index [BMI], waist/hip ratio), PH, and 16 singlenucleotide polymorphisms (SNPs) associated with T2D on T2D variability in Mexico, comparing 1234 non-diabetic controls and 1219 diabetic patients. To replicate the data, a case-control (n = 2904) and a cross-sectional (n = 1901) study were also included. In a multivariate logistic regression model, all factors accounted for only 27.3% of T2D variability: SNPs (8.4%); PH (11.8%) and obesity (7.1%). These factors contributed more in men (33.2%) than in women (25%), specifically when the disease was diagnosed before the age of 46 (46.7% vs. 30%). Genes played a substantially more important role in men than in women (14.9% vs. 5.5%), while obesity and PH played a similar role in both genders. Genes and PH appeared to play a greater role than obesity in T2D. However, obesity contribution was calculated at the time of recruitment and may be underestimated in patients because the BMI decreased linearly with the number of years with the disease. The data suggest that sexual hormones may play important roles in genes that are associated with T2D. The aetiology of type 2 diabetes (T2D) includes factors such as genes, genetic predisposition, ethnicity, poor nutrition, sedentary lifestyle, obesity, and dyslipidaemia 1. Several family-based studies of disease heritability have indicated that T2D is strongly heritable 2-4 , and the heritability is on average 25% 5. However, insufficient information exists on the heritability of T2D in non-twin families, and little is known regarding how much of this heritability is due to genes and other heritable factors, such as epigenetic factors 6. Historical studies of linkage, candidate genes, and genome-wide association studies (GWAS) have discovered more than 100 variants of genes associated with T2D 7,8. However, the influence of these genes on the disease is unclear. Based on their low individual odds ratios (ORs), most genes have very little influence on the development of the disease 8. According to the results of a European case-control study, only approximately 10% of the T2D variability can be explained by T2D-susceptible loci 9-11. Obesity is a modifiable factor that is clearly associated with the development of the disease. It is well known that the risk of T2D increases linearly as the body mass index (BMI) increases 12. In fact, obesity has been promoted as the main risk factor for diabetes 13. However, the relationship between T2D and

Parental History of Type 2 Diabetes Mellitus: A Lurking Genetic Threat

Journal of Advances in Medicine and Medical Research

Type-2 Diabetes Mellitus (T2DM) is presently the fastest growing disease and has been recognized to be caused by a collision between inherited parental genes and the environment. The current prevalence in Pakistan of type-2 diabetes mellitus is 26.3%. Out of them 19.2% had disease two to three decades back while 7.1% are recently diagnosed cases. Worldwide burden of disease was 415 million in 2015 and this number will increase to 642 million by 2040. Parental history of diabetes mellitus is a chief reason for the development of T2DM in children, but whether this association derives from shared genetic or environmental factors is unclear. Persistent high blood glucose levels can result in drastic outcomes like Diabetic Ketoacidosis and Hyperosmolar non ketotic syndrome. Genome-wide association analyses have uncovered multiple genomic regions associated with T2DM, but identification of the causal variants remains a challenge. This review will discuss the approach of diagnosing T2DM by...