Excess maternal history of diabetes in Caucasian and Afro-origin non-insulin-dependent diabetic patients suggests dominant maternal factors in disease transmission

Young, Catherine A.; Kumar, S; Young, M. J.; Boulton, A. J. M.

doi:10.1016/0168-8227(94)01058-8

Cited by 31 publications

(22 citation statements)

References 6 publications

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“…There is a strong evidence to suggest insulin resistance is genetically determined with a strong familial and environmental component [33,34,35,36,37]. Insulin resistance has a predilection for certain ethnic groups [13,16,17,24,36,37].…”

Section: Discussionmentioning

confidence: 99%

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Insulin sensitivity and cardiovascular risk factors in hypertensive and normotensive native Ghanaians

et al. 2003

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Aims/Hypothesis. The objective of this study was to examine the relationships among insulin and insulin sensitivity and risk factors for cardiovascular diseases in native Ghanaians with and without hypertension. Methods. We measured the anthropometric parameters, systolic and diastolic blood pressure, fasting serum triglycerides, cholesterol and high-density lipoprotein cholesterol and fasting and stimulated glucose, insulin and C-peptide of 200 Ghanaian subjects, who were between 25 to 74 years of age, and residing in the Accra Metropolitan area. Serum glucose, C-peptide and insulin concentrations were measured at baseline (fasting) and also 2 h after 75 gm oral glucose drink. Homeostasis model assessment was used to measure insulin resistance. Hypertension was defined as a blood pressure higher than 140/90 mmHg.Results. There were 53 subjects with hypertension (HBP) and 147 subjects with normal blood pressure (NBP). The mean BMI, waist circumference and waist-to-hip circumference ratio for HBP and NBP subjects were 27.4±0.8, 24.8±0.4 kg/m 2 ; 89.8±11.7, 81.1±0.9 cm; and 0.87±0.08, 0.82±0.08 respectively, (p<0.05). The fasting and 2-h plasma glucose concentrations in HBP and NBP subjects were 5.5±0.2, 7.2±0.3 mmol/l and 5.2±01, 6.8±0.2 mmol/l respectively (p>0.05). The corresponding fasting and 2-h insulin concentrations were 10.0±0.7, 8.0±0.4 uU/ml and 47.3±3.7, 37.3±2.5 uU/ml respectively (p<0.05). The insulin resistance index (HOMA-IR) in the HBP and the NBP groups were 2.49±0.2 and 1.95±0.13 (p<0.05). The two groups had similar fasting and stimulated C-peptide, lipids and HDL concentrations. Correlations were found between blood pressure and the concentrations of lipids, HDL, fasting and stimulated insulin and C-peptide, and between fasting insulin and HOMA-IR with lipids and HDL concentrations. On multiple regression analysis, fasting insulin and HOMA-IR did not influence blood pressure variations significantly. Conclusions/interpretation. We found clustering of hyperinsulinaemia, insulin resistance and truncal obesity in hypertensive Ghanaian subjects but dissociation between insulin resistance, hypertension and atherogenic lipid and lipoprotein profile. [Diabetologia (2003) 46:949-955] Keywords Insulin sensitivity, blood pressure, lipids, lipoproteins, hypertension, ghanaians, insulin resistance.

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Section: Discussionmentioning

confidence: 99%

“…Insulin resistance has a predilection for certain ethnic groups [13,16,17,24,36,37]. In this regard, previous studies found greater hyperinsulinaemia and insulin resistance in African-Americans [18, 24], Ghanaians [37], Afro-Caribbeans [32,33], Pima Indians…”

Section: Discussionmentioning

confidence: 99%

Insulin sensitivity and cardiovascular risk factors in hypertensive and normotensive native Ghanaians

et al. 2003

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“…In the Framingham population, maternal and paternal diabetes conferred equal risk for overt type 2 diabetes among offspring in contrast to some (13)(14)(15)(16)(17)(18)(19)(20), but not all (10,(21)(22)(23), prior studies of parental diabetes transmission. However, offspring with maternal diabetes were more likely to have milder degrees of impaired glucose homeostasis compared with offspring with paternal diabetes, with 60-80% maternal excess relative odds for exceeding a fasting glucose threshold of 6.1 mmol/l, a 2-h postchallenge glucose level of 7.8 mmol/l, or both.…”

Section: Discussionmentioning

confidence: 99%

“…Family studies have estimated that risk for diagnosed type 2 diabetes increases approximately two-to fourfold when one or both parents are affected (10)(11)(12)(13)(14). In addition, some (13)(14)(15)(16)(17)(18)(19)(20) but not all (10,(21)(22)(23) studies suggest that offspring whose mothers had diabetes are more likely to develop diabetes themselves compared with offspring whose fathers had diabetes. A variety of hypotheses have been advanced to explain this apparent excess maternal transmission of diabetes, including unique maternal genetic and environmental effects (23).…”

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confidence: 99%

Parental transmission of type 2 diabetes: the Framingham Offspring Study.

2000

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Study of parental transmission of diabetes provides insight into the relative contributions of underlying maternal and paternal influences. We estimated risk for type 2 diabetes and milder degrees of glucose intolerance associated with parental diabetes among subjects of the population-based Framingham Offspring Study, in which participants are primarily Caucasian and at relatively low risk for diabetes and for which both parental and offspring phenotypes were ascertained by direct examination. Parental diabetes, assessed over 40 years of biennial follow-up, was defined by use of hypoglycemic drug therapy or a casual plasma glucose level ≥11.1 mmol/l at any examination. Offspring glucose tolerance, assessed over 20 years of quadrennial follow-up, was defined by fasting plasma glucose levels ≥7.8 mmol/l at any two examinations, use of hypoglycemic drug therapy at any examination, or with a 75-g oral glucose tolerance test (1980 World Health Organization criteria) at the most recent examination. We calculated odds ratios (ORs) and 95% CIs for offspring glucose tolerance status using generalized estimating equations to account for differential correlations within and between families. The 2,527 offspring came from 1,303 nuclear families, of which 77.6% had two or more siblings per family and in which the prevalence of parental diabetes was 24.6%. The mean offspring age was 54 years (range 26-82), 53% were women, 8.6% had diabetes, 11.4% had impaired glucose tolerance, 76.3% had no parental diabetes, 10.5% had maternal diabetes, 11.5% had paternal diabetes, and 1.7% had bilineal diabetes. Relative to individuals without parental diabetes, the age-adjusted ORs (95% CI) for offspring type 2 diabetes or abnormal glucose tolerance (fasting plasma glucose ≥6.1 mmol/l or 2-h postchallenge glucose tolerance ≥7.8 mmol/l) among individuals with maternal diabetes were 3.4 (2.3-4.9) and 2.7 (2.0-3.7), respectively; among individuals with paternal diabetes were 3.5 (2.3-5.2) and 1.7 (1.2-2.4), respectively; and among individuals with bilineal diabetes were 6.1 (2.9-13.0) and 5.2 (2.6-10.5), respectively. Although maternal and paternal diabetes conferred equivalent risk for offspring type 2 diabetes, offspring with maternal diabetes were slightly more likely to have abnormal glucose tolerance compared with those with paternal diabetes (OR 1.6, 95% CI 1.1-2.4). Offspring with maternal diabetes and an age of onset of <50 years had marked increased risk for both type 2 diabetes (9.7, 4.3-22.0) and abnormal glucose tolerance (9.0, 4.2-19.7). We conclude that risk ratios for offspring type 2 diabetes are consistent with a simple additive risk model, where risk when both parents are affected equals the sum of risk when either parent is affected. For maternal diabetes to confer excess risk for mild but not overt glucose intolerance, offspring of diabetic fathers may transit abnormal to impaired glucose tolerance relatively quickly, or diabetic mothers may transmit risk for a mild slowly progressive form of abnormal glucose tolerance in...

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“…The existence of excess maternal transmission of type 2 diabetes is still in controversial issues. Although the majority of studies suggest that excess maternal transmission occurs [6,7,[11][12][13][14][15][16][17][18][19], however, a few studies refute this finding [20][21][22]. Recently, the Framingham Offspring Study suggested equivalent maternal and paternal effects on risk for offspring diabetes [20].…”

Section: Introductionmentioning

confidence: 99%