Alterations of maternal metabolism in normal and diabetic pregnancies: Differences in insulin-dependent, non-insulin-dependent, and gestational diabetes

Hollingsworth, Dorothy R.

doi:10.1016/0002-9378(83)90822-0

Cited by 78 publications

(37 citation statements)

References 30 publications

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“…These results are consistent with clinical and experimental observations that estrogen excesses, as in pregnancy [2,3], trans-sexuality [4], and during menstrual cycles [5], or estrogen deficiencies as in aromatase deficient [6] and OVX animals [7], cause insulin resistance. Moreover, a selective ER-α antagonist, MPP, diminished the beneficial effect of E2 at 10 -8 M on glucose uptake.…”

Section: Discussionsupporting

confidence: 90%

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Estrogen Receptor .ALPHA. Regulates Insulin Sensitivity through IRS-1 Tyrosine Phosphorylation in Mature 3T3-L1 Adipocytes

2006

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Abstract. There are many clinical and experimental reports demonstrating that estrogens and insulin interact when affecting their target organs. Estrogen receptors consist of two isoforms, estrogen receptors-alpha (ER-α) and -beta (ER-β), but their roles in insulin-induced glucose uptake in mature adipose tissue have yet to be clarified. To evaluate the roles of ER-α, expressed predominantly in adipocytes, we have investigated the effects of estradiol (E2), an ER-α selective agonist (PPT), and its selective antagonist (MPP) on glucose uptake and insulin action in 3T3-L1 adipocytes. 3T3-L1 adipocytes were exposed to E2 or PPT and/or MPP at different concentrations. The cells were then subjected to 2-deoxy-D-glucose transport assay, western blot analysis, or RT-PCR analysis. Treatment of these cells with E2 or PPT resulted in biphasic effects on glucose transport, that is high (10 -5 M or 3 × 10 -6 M each) and low (10 -8 M) doses produced inhibition and stimulation, respectively. The favorable effect observed at 10 -8 M of E2 was diminished by treatment with MPP. Western bolt analysis revealed that these effects of E2, PPT and MPP paralleled the level of IRS-1 tyrosine phosphorylation. However, IRS-1 serine phosphorylation, suppressor of cytokine signaling (SOCS)-1,-2,-3 and protein tyrosine phosphatase 1B (PTP1B) expression did not change compaired to control subjects. Our data clearly show that ER-α contributes to insulin stimulated glucose uptake through regulation of the tyrosine phosphorylation of IRS-1 protein.

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Section: Discussionsupporting

confidence: 90%

“…In clinical studies, high concentrations of estrogens, as in pregnancy [2,3], trans-sexuality [4] and during menstrual cycles [5], appear to contribute to the development of insulin resistance. On the other hand, there is considerable evidence against adverse effects of estrogens on glucose metabolism and some for beneficial actions of estrogen.…”

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confidence: 99%

Estrogen Receptor .ALPHA. Regulates Insulin Sensitivity through IRS-1 Tyrosine Phosphorylation in Mature 3T3-L1 Adipocytes

2006

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“…In contrast, women who develop gestational diabetes or who have Type II diabetes during pregnancy exhibit the same degree of insulin resistance in the late stages of pregnancy, but a lower insulin secretory response, than do nondiabetic women [10]. As a result, the intrauterine environment in gestational diabetes is characterized by increased concentrations of glucose, amino acids and lipids in the maternal circulation, greater delivery of these nutrients to the fetus, raised fetal insulin secretion, and accelerated fetal growth [11,12]. Because differentiation of adipose tissue and storage of triglycerides begins during the third trimester of pregnancy [13], the effect of diabetes at this point in fetal development is to hasten the accumulation of fat in the fetus and results in infants that are both heavier and fatter than infants born to nondiabetic women [14].…”

Section: : 1157±1162]mentioning

confidence: 99%

Maternal diabetes status does not influence energy expenditure or physical activity in 5-year-old Pima Indian children

et al. 1998

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The Pima Indians of Arizona have the world's highest reported prevalence of diabetes [1,2]; after 35 years of age, 50 % of the population is reported to have diabetes [1]. We have found that at each age, both the prevalence and incidence of diabetes is higher than earlier in our studies, resulting in more people with diabetes at earlier ages. As the age of onset of diabetes decreases, more women of childbearing age have Type II (non-insulin-dependent) diabetes or are at risk of developing gestational diabetes, which results in larger babies at birth [3±5]. Obesity, in turn, predisposes the children of women with diabetes to developing diabetes themselves, thus resulting in a ªcross-generational vicious cycleº [6] whereby successive generations of women are at greater risk of already being obese and having diabetes at childbearing age than the preceding generation.In healthy, nondiabetic women, normal pregnancy is associated with insulin resistance, hyperinsulin- Diabetologia (1998) Summary Children of women who have diabetes during pregnancy are more likely to become obese by early adulthood than those of women with normal glucose tolerance during pregnancy. Obesity can result from either excess food intake, low levels of energy expenditure or both. In our study, we tested whether maternal diabetes status influences total energy expenditure (TEE by doubly labelled water), resting metabolic rate (RMR by ventilated hood) and physical activity level (PAL = TEE/RMR and assessed by activity questionnaire). Measurements were taken in 88 5-year-old Pima Indian children, 24 children of women with diabetes (2-h plasma glucose ³ 11.1 mmol/l) diagnosed before or during pregnancy and 64 children of women with normal glucose tolerance (2-h plasma glucose < 7.8 mmol/l during pregnancy and no prior history of abnormal glucose tolerance). Although birth weight was higher in children of diabetic than of nondiabetic women (mean ± SD; 3.8 ± 0.6 vs 3.5 ± 0.4 kg, p < 0.03), there were no differences in weight (26.4 ± 6.9 vs 24.2 ± 5.6 kg) or per cent body fat ( 18 O dilution; 33 ± 8 vs 31 ± 8 %) between the groups at 5 years of age. There was no difference in TEE (6508 ± 1109 vs 6175 ± 942 kJ/d) or in RMR (4674 ± 786 vs 4483 ± 603 kJ/d) expressed as absolute values or after adjustment for weight and sex (TEE) or fat-free mass, fat mass, and sex (RMR). Physical activity level was also similar between the groups (1.40 ± 0.12 vs 1.38 ± 0.12). These results suggest that maternal diabetes status does not influence energy expenditure in the children by 5 years of age. Thus the greater obesity seen at older ages in the children of women with diabetes could be due to excess energy intake. Alternatively, if energy expenditure does have a role in the aetiology of obesity in these children, perhaps it does so only in older children. [Diabetologia (1998

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“…Gestational diabetes mellitus (GDM) occurs in 2 ± 4% of all pregnancies and is characterized by a pronounced decrease in insulin sensitivity and an insuf®cient insulin secretion leading to abnormal glucose tolerance during pregnancy (Hollingsworth, 1983;Buchanan et al, 1990;National Diabetes Data Group, 1979;American Diabetes Association, 1993;Ku Èhl, 1975;Ku Èhl et al, 1984). The advantage of a high-carbohydrate, low-fat diet in treatment of type 2 diabetes has been questioned, due to carbohydrate-induced increase of triacylglycerol concentrations (American Diabetes Association, 1987;Medical Advisory Committee, 1982;Pedersen O, 1994;Coulston et al, 1987Coulston et al, , 1988.…”

Section: Introductionmentioning

confidence: 99%

Effect of a high monounsaturated fatty acid diet on blood pressure and glucose metabolism in women with gestational diabetes mellitus

Lauszus¹,

Rasmussen

Henriksen

et al. 2001

Eur J Clin Nutr

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Objective: The effect of a diet rich in monounsaturated fatty acids (MUFA) on blood pressure, glycemic control, lipids and insulin sensitivity was evaluated in women with gestational diabetes mellitus. Design and methods: A randomized, unpaired diet intervention was performed in 27 women with gestational diabetes mellitus in an outpatient clinic. After randomization the women received either a high-carbohydrate diet (H-CHO) or a high-MUFA diet (H-MUFA) from the 33rd gestational week of pregnancy. Outcome measures were 24 h ambulatory blood pressure, blood lipids, glycemic control and insulin sensitivity estimated by an intravenous glucose tolerance test. Results: The 24 h diastolic blood pressure increased more in the H-CHO group than in the H-MUFA group (P`0.04). Conclusions: After 5 weeks of treatment with a MUFA-enriched diet, no increase in 24 h diastolic blood pressure and no adverse effects on blood lipids were seen. The favorable effect on the blood pressure by the MUFA diet is a possible non-medication treatment. The H-MUFA diet had no advantage to the H-CHO diet in ameliorating the decline of insulin sensitivity in third term of pregnancy in GDM.

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Alterations of maternal metabolism in normal and diabetic pregnancies: Differences in insulin-dependent, non-insulin-dependent, and gestational diabetes

Cited by 78 publications

References 30 publications

Estrogen Receptor .ALPHA. Regulates Insulin Sensitivity through IRS-1 Tyrosine Phosphorylation in Mature 3T3-L1 Adipocytes

Estrogen Receptor .ALPHA. Regulates Insulin Sensitivity through IRS-1 Tyrosine Phosphorylation in Mature 3T3-L1 Adipocytes

Maternal diabetes status does not influence energy expenditure or physical activity in 5-year-old Pima Indian children

Effect of a high monounsaturated fatty acid diet on blood pressure and glucose metabolism in women with gestational diabetes mellitus

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