Erythrocytosis in offspring of mothers with Type 1 diabetes—are factors other than insulin critical determinants?

Nelson, Scott M.; Freeman, Dilys J.; Sattar, Naveed; Lindsay, Robert

doi:10.1111/j.1464-5491.2009.02797.x

Cited by 14 publications

(9 citation statements)

References 35 publications

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“…OT1DM were markedly heavier with z scores of birth weight 1.8 SD above the expected for the background population. Where available, cord insulin and leptin were increased in OT1DM (supplementary Table A1), in keeping with the larger dataset from the original cohort (8), while differences in hematocrit (9), CRP (10), and adiponectin previously found in the larger set (11) were in similar directions, although not formally significant in this subgroup (supplementary Table A1).…”

Section: Resultssupporting

confidence: 69%

“…We have described a number of hormonal and other changes at birth in this cohort of OT1DM. Cord insulin, leptin, and birth weight (8) are markedly raised, hematocrit (9) and CRP (10) are more modestly increased, and adiponectin decreased (11). While several of these changes are intercorrelated, insulin and leptin are not particularly strongly related in OT1DM ( r = 0.22) (8).…”

Section: Discussionmentioning

confidence: 99%

“…Further, we used the extensive phenotyping of the cohort at birth to examine which of a number of changes previously identified at birth in this cohort—most notably raised birth weight, fetal hyperinsulinemia, and fetal hyperleptinemia (8), but also increased cord hematocrit (9), C-reactive protein (CRP) (10), and reduced adiponectin (11)—might be associated with risk of offspring obesity.…”

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confidence: 99%

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Programming of Adiposity in Offspring of Mothers With Type 1 Diabetes at Age 7 Years

et al. 2010

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OBJECTIVEThe goals of this study were to examine the influence of maternal type 1 diabetes during pregnancy on offspring adiposity and glucose tolerance at age 7 years and to assess whether metabolic factors at birth (neonatal leptin and insulin) predict adverse outcomes.RESEARCH DESIGN AND METHODSWe examined 100 offspring of mothers with type 1 diabetes (OT1DM) and 45 offspring of control mothers. Mothers had previously been recruited during pregnancy, and, where possible, birth weight, umbilical cord insulin, and leptin were measured. Children were classed as overweight and obese using age-specific reference ranges.RESULTSOT1DM had similar height (control, 1.25 ± 0. 06 m; OT1DM, 1.24 ± 0.06 m; P = 0.81) but were heavier (control, 25.5 ± 3.8 kg; OT1DM, 27.1 ± 5.7 kg; P = 0.048) and had an increased BMI (control, 16.4 kg/m2; OT1DM, 17.4 ± 2.6 kg/m2, P = 0.005). Waist circumference (control, 56.0 ± 3.7 cm; OT1DM, 58 ± 6.8 cm; P = 0.02) and sum of skinfolds were increased (control, 37.5 ± 17.0 mm [n = 42]; OT1DM, 46.1 ± 24.2 mm [n = 91]; P = 0.02), and there was a marked increase in the prevalence of overweight and obese children (OT1DM, 22% overweight and 12% obese; control, 0% overweight and 7% obese; χ2 P = 0.001). Glucose tolerance was not different compared with that in control subjects. BMI at age 7 years correlated with cord leptin (OT1DM, r = 0.25; n = 61, P = 0.047), weakly with adjusted birth weight (r = 0.19; P = 0.06) and hematocrit (r = 0.25; n = 50, P = 0.07), but not cord insulin (OT1DM, r = −0.08; P = 0.54).CONCLUSIONSOT1DM are at increased risk of overweight and obesity in childhood. This risk appears to relate, in part, to fetal leptin and hematocrit but not insulin.

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Section: Resultssupporting

confidence: 69%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Programming of Adiposity in Offspring of Mothers With Type 1 Diabetes at Age 7 Years

et al. 2010

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“…Plasma insulin, 32-33 split proinsulin, proinsulin, leptin, IGF-I, adiponectin, plasma total cholesterol, triglycerides, nonesterified fatty acid, VLDL cholesterol, LDL cholesterol, HDL cholesterol, C-reactive protein (CRP), intercellular adhesion molecule (ICAM)-1, and interleukin (IL)-6 were assayed as previously described (13,21–24). In particular, IGF-I was assayed by chemiluminescence immunoassay (Nichols Institute Diagnostics, San Juan Capistrano, CA) using standards referenced to the World Health Organization 1st International Reference Reagent 1988 (IGF-1 87/518).…”

Section: Methodsmentioning

confidence: 99%

Placental Structure in Type 1 Diabetes

et al. 2009

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OBJECTIVEAlteration of placental structure may influence fetal overgrowth and complications of maternal diabetes. We examined the placenta in a cohort of offspring of mothers with type 1 diabetes (OT1DM) to assess structural changes and determine whether these were related to maternal A1C, fetal hematocrit, fetal hormonal, or metabolic axes.RESEARCH DESIGN AND METHODSPlacental samples were analyzed using stereological techniques to quantify volumes and surface areas of key placental components in 88 OT1DM and 39 control subjects, and results related to maternal A1C and umbilical cord analytes (insulin, leptin, adiponectin, IGF-I, hematocrit, lipids, C-reactive protein, and interleukin-6).RESULTSIntervillous space volume was increased in OT1DM (OT1DM 250 ± 81 cm3 vs. control 217 ± 65 cm3; P = 0.02) with anisomorphic growth of villi (P = 0.025). The placentas showed a trend to increased weight (OT1DM 690 ± 19 g; control 641 ± 22 g; P = 0.08), but villous, nonparenchymal, trophoblast, and capillary volumes did not differ. Villous surface area, capillary surface area, membrane thickness, and calculated morphometric diffusing capacity were also similar in type 1 diabetic and control subjects. A1C at 26–34 weeks associated with birth weight (r = 0.27, P = 0.03), placental weight (r = 0.41, P = 0.0009), and intervillous space volume (r = 0.38, P = 0.0024). In multivariate analysis of cord parameters in OT1DM, fetal IGF-I emerged as a significant correlate of most components (intervillous space, villous, trophoblast, and capillary volumes, all P < 0.01). By contrast, fetal insulin was only independently associated with capillary surface area (positive, r2 = 6.7%; P = 0.02).CONCLUSIONSThere are minimal placental structural differences between OT1DM and control subjects. Fetal IGF-I but not fetal insulin emerges as a key correlate of placental substructural volumes, thereby facilitating feedback to the placenta regarding fetal metabolic demand.

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“…‘Emerging’ factors that seem to be related to the absence of anemia in CKD patients have recently been described, such as IGF-1 [17], insulin [18] and renin [19]. The study by Shih et al [17] included patients with erythrocytosis on HD and found that IGF-1 and insulin can act as stimulants of erythropoiesis in these patients, since they had elevated levels of these factors and erythrocytosis even with suppressed eEPO levels.…”

Section: Discussionmentioning

confidence: 99%

Factors Related to the Absence of Anemia in Hemodialysis Patients

et al. 2011

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Background: A small number of hemodialysis (HD) patients have normal hemoglobin (Hb) levels without the need for erythropoiesis-stimulating agents (ESAs). The factors associated with this condition have been little studied. The objective of this prospective study was to determine these factors in a prevalent population of HD patients. Materials and Methods: All patients who had normal Hb levels and who had not received ESAs in the last 6 months (non-ESA group) were included. Epidemiological and laboratory data were collected and we performed an abdominal ultrasound to assess hepatic and renal cysts. This group was compared to a control group of 205 prevalent HD patients on ESA therapy (control group). Results: We included 45 patients (16% from the whole group) in the non-ESA group. In this group, there was a higher proportion of men (76.5 vs. 61%), patients were younger (61.1 ± 14.7 vs. 67.5 ± 15.2 years), had a longer duration of renal replacement therapy (RRT) (9.4 ± 8.3 vs. 5.3 ± 5.8 years) and had a higher prevalence of adult polycystic kidney disease (APKD) and hepatitis C virus (HCV) liver disease (42.2 vs. 10.2%), p < 0.01. In the non-ESA group, HCV+ patients had a lower prevalence of APKD (2.2 vs. 38.4%) and hepatic cysts (2.2 vs. 19.2%), but significantly higher endogenous erythropoietin levels (55.8 ± 37.1 vs. 30.9 ± 38.4 mU/ml). No significant differences in anemia, iron metabolism, insulin, IGF-1 and renin were found between non-ESA and control groups. Non-ESA patients had a significantly higher number of renal (90.6 vs. 36.5%) and hepatic cysts (12.5 vs. 3.4%), and these were also larger in size (3.3 ± 2.4 vs. 1.5 ± 0.8 cm). In the multivariate Cox analysis, independent predictor factors for absence of anemia in HD patients were number of renal cysts >10 cysts (95% CI 1.058–1.405; p = 0.00), HCV+ liver disease (95% CI 1.147–1.511; p = 0.05) and time on RRT (95% CI 1.002–1.121; p = 0.05). Conclusions: The absence of anemia in HD patients is not infrequent. Its frequency is higher in men and younger patients with long-term RRT, in patients with HCV+ liver disease and in APKD. It is associated with increased endogenous erythropoietin production and the presence of renal and hepatic cysts.

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Erythrocytosis in offspring of mothers with Type 1 diabetes—are factors other than insulin critical determinants?

Cited by 14 publications

References 35 publications

Programming of Adiposity in Offspring of Mothers With Type 1 Diabetes at Age 7 Years

Programming of Adiposity in Offspring of Mothers With Type 1 Diabetes at Age 7 Years

Placental Structure in Type 1 Diabetes

Factors Related to the Absence of Anemia in Hemodialysis Patients

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