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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interrelationships between magnesium and carbohydrate metabolism have regained considerable interest over the last few years. Insulin secretion requires magnesium: magnesium deficiency results in impaired insulin secretion while magnesium replacement restores insulin secretion. Furthermore, experimental magnesium deficiency reduces the tissues sensitivity to insulin. Subclinical magnesium deficiency is common in diabetes. It results from both insufficient magnesium intakes and increase magnesium losses, particularly in the urine. In type 2, or non-insulin-dependent, diabetes mellitus, magnesium deficiency seems to be associated with insulin resistance. Furthermore, it may participate in the pathogenesis of diabetes complications and may contribute to the increased risk of sudden death associated with diabetes. Some studies suggest that magnesium deficiency may play a role in spontaneous abortion of diabetic women, in fetal malformations and in the pathogenesis of neonatal hypocalcemia of the infants of diabetic mothers. Administration of magnesium salts to patients with type 2 diabetes tend to reduce insulin resistance. Long-term studies are needed before recommending systematic magnesium supplementation to type 2 diabetic patients with subclinical magnesium deficiency.
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PMID:[Magnesium and glucose metabolism]. 809 58

Maternal diabetes mellitus (types 1 and 2) is the most chronic prevalent medical condition affecting the pregnant population and is associated with a less satisfactory pregnancy outcome for both mother and infant when compared with the non-diabetic population. Most reports have focused on women with type 1 disease, type 2 disease being perceived as a less serious condition. However, type 2 disease is far more common (and is increasing) in some areas of the UK, especially where there is a high proportion of women from the Indian subcontinent. This paper shows that pregnancy complicated by type 2 diabetes mellitus is a high-risk state, with miscarriage and congenital malformations almost twice that seen in type 1 disease. These adverse outcomes are contributed to by poor attendance for pre-pregnancy care, later booking for antenatal clinic and poor glycaemic control at booking. Offspring of pregnancies complicated by type 2 diabetes are more likely to be delivered before 37 weeks gestation and be large in size for gestational age. We must dispel the myth, in women of childbearing age and in their healthcare providers, that diabetes treated with diet and/or tablets (type 2) is a less serious problem than type 1 disease.
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PMID:Pregnancy outcome in women with type 2 diabetes mellitus needs to be addressed. 1107 May 63

Maternal and fetal complications are increased when pregnancy is complicated by diabetes, and this may be further influenced by racial and cultural differences. We examined fetal and maternal outcomes in Indo-Asian and Caucasian women attending the same antenatal diabetes service to see if there were any differences. Women with diabetes mellitus (type 1, type 2 and gestationally-acquired disease) complicating pregnancy, registered at the combined diabetes/antenatal clinic of this University teaching hospital over the period 1990-1998 were included. Fetal outcomes examined were miscarriage <24 weeks, stillbirths, neonatal deaths up to 28 days of life, perinatal mortality, congenital malformations and size for gestational age. Maternal outcomes examined were rates of caesarean section and vaginal deliveries, and number of pre-term deliveries <37 completed weeks of gestation. Outcomes for Indo-Asian and Caucasian women were similar, with a take-home baby rate of 96% and 92%, respectively. There was no perinatal mortality in Indo-Asian women, who were more likely to have a vaginal delivery and less likely to have a baby large for gestational age. Pregnancies complicated by type 2 diabetes in both groups pose the greatest threat to a successful pregnancy outcome. Indo-Asian and Caucasian women attending the same antenatal diabetes service have comparable outcomes. Attendance for pre-pregnancy care needs to be encouraged to combat the high early pregnancy loss and congenital malformation rate identified, particularly in those with type 2 disease, irrespective of ethnicity.
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PMID:Fetal and maternal outcomes in Indo-Asian compared to caucasian women with diabetes in pregnancy. 1111 May 88

The recognition of insulin resistance as a principal factor in the pathogenesis of polycystic ovarian syndrome (PCOS) has led to the use of insulin-lowering agents, also called 'insulin-sensitizing drugs', for its treatment. The most extensively studied insulin-lowering agent in the treatment of PCOS is metformin: an oral antihyperglycaemic agent used initially in the treatment of type 2 diabetes mellitus. Metformin is effective in the treatment of PCOS-related anovulation and infertility. Moreover, preliminary evidence indicates that metformin may also be effective in decreasing the risk of early spontaneous miscarriage in women with PCOS. Metformin also appears to induce cardioprotective effects on serum lipids as well as plasminogen activator inhibitor (PAI)-1 and may decrease the risk of development of type 2 diabetes. The highly promising therapeutic profile of metformin is related to the role of this agent in controlling an important aetiologic factor in the pathogenesis of PCOS: hyperinsulinaemia.
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PMID:Should patients with polycystic ovarian syndrome be treated with metformin? 1220 7

Metformin is a common treatment for women who have insulin resistance manifesting as type 2 diabetes or polycystic ovarian syndrome (PCOS). With an increasing number of these patients conceiving, it is expected that the use of metformin in and around the time of pregnancy will increase. This article reassesses the mechanisms, safety, and clinical experience of metformin use in obstetrics and gynecology. Metformin is an attractive therapeutic option because administration is simple, hypoglycemia rare, and weight loss promoted. There is a large volume of research supporting the use of metformin treatment in diabetes mellitus, androgenization, anovulation, infertility, and recurrent miscarriage. Although metformin is known to cross the placenta, there is, as yet, no evidence of teratogenicity. Metformin has an array of complex actions, accounting for the varied clinical roles, many of which are still to be fully evaluated. Much research is still needed.
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PMID:Metformin in obstetric and gynecologic practice: a review. 1475

The purpose is to identify maternal and prenatal risks factors for placental vascular disorders. We excluded biologic and epidemiological data which are discussed in another chapter. Maternal risks factors are pre-existing vascular systemic diseases. Systemic lupus erythematosus (antiphospholipid antibodies are studied in another chapter) is a classical disease associated with unfavorable outcome, particularly when the disease is not quiescent and if the patient has a history of previous poor outcome. Obstetricians' awareness of the influence of inflammatory bowel diseases on pregnancy and fetal outcome is quite poor. These diseases, if they are not quiescent, can induce deleterious perinatal effects. Type 1 or even type 2 diabetes mellitus increases the risk of preeclampsia or hypertension in pregnancy, particularly when there is poor glycemic control early in pregnancy. The duration of type 1 diabetes affects the outcome of pregnancy more than type 2. Smoking during pregnancy is associated with many adverse events including spontaneous abortion, low birth weight and placental abruption. There are data about the dose-response relationship between the number of cigarettes smoked per day and the risk of abortion. Smoking during pregnancy is also protective against preeclampsia and this apparent paradox suggests the complexity of what is called vascular placental pathology. There is a significant relationship between pejorative perinatal vascular outcome and the non quiescence of renal disease. Mid-trimester uterine artery Doppler combining bilateral notches and increased uterine resistance index is the best criterion to predict the placental vascular risk of the pregnancy. Some promising studies suggest the feasibility of uterine Doppler ultrasound screening early in the pregnancy during the first trimester. Large studies are required to confirm this practice. Uterine artery Doppler in combination with other tests (elevated maternal serum hCG or ambulatory 24-hour blood pressure monitoring at 22 weeks gestation) could be a more efficient predictor of vascular complications. A large-scale evaluation is necessary before recommendations can be made. Multiple pregnancies increase the risk of preeclampsia 2- or 3-fold (RR 2.62; 95% CI: 2.03-3.38). A history of preeclampsia is the strongest predictor of unfavorable outcome for the second pregnancy.
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PMID:[Maternal and obstetrical risk factors of placental vascular pathology (biologic and epidemiological data excluded)]. 1502 85

Polycystic ovarian syndrome is a hormonal disturbance that results in a collection of symptoms and has wide-ranging health implications. There is evidence that it may run in families, and it is associated with the development of type 2 diabetes and recurrent miscarriage. Diagnosis involves eliminating other potential conditions, while treatment aims to manage individual symptoms rather than provide a cure.
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PMID:Diagnosis and treatment of polycystic ovarian syndrome. 1585 Feb 63

Coffee is a complex mixture of chemicals that provides significant amounts of chlorogenic acid and caffeine. Unfiltered coffee is a significant source of cafestol and kahweol, which are diterpenes that have been implicated in the cholesterol-raising effects of coffee. The results of epidemiological research suggest that coffee consumption may help prevent several chronic diseases, including type 2 diabetes mellitus, Parkinson's disease and liver disease (cirrhosis and hepatocellular carcinoma). Most prospective cohort studies have not found coffee consumption to be associated with significantly increased cardiovascular disease risk. However, coffee consumption is associated with increases in several cardiovascular disease risk factors, including blood pressure and plasma homocysteine. At present, there is little evidence that coffee consumption increases the risk of cancer. For adults consuming moderate amounts of coffee (3-4 cups/d providing 300-400 mg/d of caffeine), there is little evidence of health risks and some evidence of health benefits. However, some groups, including people with hypertension, children, adolescents, and the elderly, may be more vulnerable to the adverse effects of caffeine. In addition, currently available evidence suggests that it may be prudent for pregnant women to limit coffee consumption to 3 cups/d providing no more than 300 mg/d of caffeine to exclude any increased probability of spontaneous abortion or impaired fetal growth.
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PMID:Coffee and health: a review of recent human research. 1650 75

Diabetes is a genetically determined metabolic disease with fasting hyperglycemia due to relative or absolute absence of insulin. With the use of exogenous insulin, successful gestations are now possible. Nevertheless, there are still severe problems associated, such as spontaneous abortion, perinatal mortality and congenital malformations. Caudal regression syndrome, disclosure of the neural tube and cardiovascular alterations are the most common malformations. Gestational diabetes can induce increased fetal corporal fat and macrosomia with hyperinsulinemia, hypoglycemic, hypoxia, metabolic acidosis and perinatal death. During adult life, diabetic mothers' children can develop obesity, glucose intolerance and type 2 diabetes. In order to study fetuses' alterations during diabetic gestations we now have animal models of diabetes. Maternal diabetes in rats alters fetal development in a very similar manner to that of humans. Although we do not accurately know the pathogenic mechanism by which diabetes produces fetuses' abnormal development, hyperglycemia and hyperketonemia had been mentioned to have predominant roles. Hyperglycemia damages DNA and increases oxidative stress and hyperketonemia increases the rate of embryo malformations. The addition of antioxidants such as C and E vitamins can reduce this damage. During adult life, diabetic rats' cubs have alterations in glucose metabolism and in reproductive function. The understanding of mechanisms by which maternal diabetes affects fetuses development, can help us to prevent complications and improve mothers' and children's life quality.
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PMID:[Effect of maternal diabetes on human and rat fetal development]. 1658 35

Obese women are characterized by similar comorbidities to men, particularly type 2 diabetes mellitus and cardiovascular diseases. Moreover, they also develop some specific problems, including fertility-related disorders and some hormone-dependent forms of cancer. The relationship between excess body fat and reproductive disturbances appears to be stronger for early-onset obesity. Early onset of obesity, particularly during adolescence, favours the development of menses irregularities, chronic oligo-anovulation and infertility in adulthood. Moreover, obesity in women can increase the risk of miscarriage and impair the outcome of assisted reproductive technologies. The main factor implicated in the association between obesity and fertility-related disorders is insulin excess, which accompanies insulin resistance. Hyperinsulinaemia may be directly responsible for the development of androgen excess, through its effects in reducing sex hormone-binding globulin synthesis and circulating concentrations, and in stimulating ovarian androgen production rates. Androgen excess, in turn, represents one of the major factors leading to altered ovarian physiology and associated ovulatory disturbances. Obesity-associated hyperleptinaemia may represent an additional factor involved in anovulation, not only through the induction of insulin resistance, but also through a direct impairment of ovarian function.
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PMID:Metabolic effects of obesity on reproduction. 1679 96


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