Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Women with gestational diabetes have a high risk for dysglycemia and metabolic syndrome. The post-partum screening evaluation allows to establish the "metabolic profile". The components of the SM must be recognized and treated. The life-style modifications are the priority. A follow-up by the general practitioner, assisted by a dietitian when it is indicated must be set up and the objectives regularly evaluated. The difficulty perceiving the long-term benefits and the changes of priority when the child is born represent specific barriers for the preventive interventions and must be identified. Specific preventive strategies to this population at high risk must be created and evaluated.
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PMID:[Gestational diabetes: what follow-up after delivery?]. 1678 92

Differentiation of the various forms of diabetes is necessary for therapeutic reasons. Typical signs of type 2 diabetes are age over 40, obesity, and other markers for metabolic syndrome, a positive famitory, gradual development of the classical symptoms, and no evidence of ketosis. It is important to distinguish this from LADA (latent autoimmune diabetes of adulthood), a form of type 1 diabetes mellitus. To establish this differential diagnosis antibody testing is employed. Antibody tests in patients with newly manifest diabetes make good sense when the clinical diagnosis is not unequivocal, that is, to distinguish it from type 2 diabetes, MODY diabetes, hereditary and secondary forms. At present, immunodiagnosis is used too often in unambiguous cases of type 1 diabetes, but too rarely in supposed type 2 diabetes. As a rule, LADA patients are GADA-positive. If MODY diabetes is suspected, a genetic examination is indicated. In patients with GDM, antibody testing with GADA makes sense, in particular in slim patients receiving insulin treatment, since these patients have a high risk for developing a postpartum diabetes already in the first years.
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PMID:[Diabetes mellitus--differential diagnosis]. 1680 91

Human diseases in adulthood are increasingly associated with growth patterns in early life, implicating early-life nutrition as the underlying mechanism. The thrifty phenotype hypothesis proposed that early-life metabolic adaptations promote survival, with the developing organism responding to cues of environmental quality by selecting an appropriate trajectory of growth. Recently, some authors have proposed that the thrifty phenotype is also adaptive in the longer-term, by preparing the organism for its likely adult environment. However, windows of plasticity close early during human development, and subsequent environmental changes may result in the selected trajectory becoming inappropriate, leading to adverse effects on health. This paradox generates uncertainty as to whether the thrifty phenotype is indeed adaptive for the offspring in humans. The thrifty phenotype should not be considered a dichotomous concept, rather it refers to the capacity of all offspring to respond to environmental information during early ontogenetic development. This article argues that the thrifty phenotype is the consequence of three different adaptive processes - niche construction, maternal effects, and developmental plasticity - all of which in humans are influenced by our large brains. While developmental plasticity represents an adaptation by the offspring, both niche construction and parental effects are subject to selection on parental rather than offspring fitness. The three processes also operate at different paces. Human offspring do not become net calories-producers until around 18 years of age, such that the high energy costs of the human brain are paid primarily by the mother, even after weaning. The evolutionary expansion of human brain volume occurred in environments characterised by high volatility, inducing strong selective pressure on maternal capacity to provision multiple offspring simultaneously. The thrifty phenotype is therefore best considered as a manipulation of offspring phenotype for the benefit of maternal fitness. The information that enters offspring phenotype during early development does not predict the likely future environment of the offspring, but rather reflects the mother's own developmental experience and the quality of the environment during her own maturation. Offspring growth trajectory thus becomes aligned with long-term maternal capacity to provision. In contemporary populations, the sensitivity of offspring development to maternal phenotype exposes the offspring to adverse effects, through four distinct pathways. The offspring may be exposed to (1) poor maternal metabolic control (e.g. gestational diabetes), (2) maternally derived toxins (e.g. maternal smoking), or (3) low maternal social status (e.g. small size). Adverse consequences of these effects may then be exacerbated by (4) exposure either to the "toxic" western environment in postnatal life, in which diet and physical activity levels are mismatched with metabolic experience in utero, or at the other extreme to famine. The rapid emergence of the epidemic of the metabolic syndrome in the 20th Century reflects the rapid acceleration in the pace of niche construction relative to the slower physiological combination of developmental plasticity and parental effects.
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PMID:The thrifty phenotype as an adaptive maternal effect. 1731 27

Gestational diabetes mellitus (GDM) should be regarded as a sentinel event in a woman's life that presents challenges and disease prevention opportunities to all providers of health care for women of reproductive age. Prediabetic risk factors are rising in prevalence and include dietary and lifestyle habits, which when superimposed on genetic predisposition contribute to the rising prevalence of type 2 diabetes and GDM. There is growing evidence that treatment of GDM matters, with a continuum of adverse pregnancy outcome risks proportional to degrees of maternal glucose intolerance. GDM in an index pregnancy increases the risk of recurrent GDM in subsequent pregnancies, and recurrence rates of up to 70% have been reported. GDM recurrence rates are influenced by maternal health characteristics and past pregnancy history. The risk of later metabolic syndrome and type 2 diabetes is increased in women with a history of GDM and women should be screened for postpartum glucose intolerance. Opportunities to prevent recurrent GDM and later type 2 diabetes require attention to risk factors and plasma glucose status with identification of impaired fasting glucose or impaired glucose tolerance.
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PMID:Recurrent gestational diabetes: risk factors, diagnosis, management, and implications. 1753 99

Among patients with metabolic syndrome (MS), atherosclerosis and abnormal fibrinolytic function are frequently present, mostly owing to an increase in plasminogen activator inhibitor-1(PAI-1). We analyze PAI-1 in pregnant women, both normal and with gestational diabetes (GDM) and postpartum regarding its correlation to MS surrogates. Clinical characteristics, glucose tolerance (100g-OGTT), lipids, PAI-1 antigen, insulin sensitivity (HOMA-S), and pancreatic beta-cell function (HOMA-B) were investigated in 34 women. Eleven had normal glucose tolerance (NGT) during pregnancy and 23 had GDM (all GAD antibodies-negative). All patients were studied at 28-34 weeks of gestation and 16-24 weeks after delivery (75 g-OGTT). Parameters of interest were determined using commercial test systems. During pregnancy, PAI-1 was not statistically different between NGT and GDM (47+/-25 ng/ml versus 47+/-28 ng/ml, p=0.9). After gestation, 19 (56%) women had NGT (11 of them from previous NGT group) and 15 (44%) had impaired glucose tolerance (IGT) or DM. The IGT (IGT+DM) group had higher PAI-1 (p=0.01), which did not decreased after delivery NGT-NGT before and after delivery (47+/-25 ng/ml versus 6+/-5 ng/ml; p<0.001), GDM-NGT (62+/-36 ng/ml versus 14+/-15 ng/ml; p=0.001) and GDM-IGT (39+/-20 ng/ml versus 27+/-23 ng/ml; p=0.15). PAI-1 levels were positively correlated (p<0.05) to total cholesterol (r(s)=0.37), triglycerides (r(s)=0.48), fasting plasma glucose (r(s)=0.52), 2-h plasma glucose in the OGTT (r(s)=0.58) and were negatively correlated (p<0.05) with HOMA-S (r(s)=-0.42) and HOMA-B (r(s)=-0.38). Fibrinolytic dysfunction is still present in GDM women and is associated with early development of IGT or T2DM. PAI correlated with surrogate markers of MS levels and may identify a group of women at risk for macroangiopathy.
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PMID:Fibrinolytic dysfunction after gestation is associated to components of insulin resistance and early type 2 diabetes in latino women with previous gestational diabetes. 1754 39

The complexity of the several pathogenic pathways that cause hypertension and vascular disease and the prolonged interval that appears to predate clinical morbidity have hindered inquiry into the association between GDM and vascular disorders. As a forme fruste of later type 2 diabetes, GDM-affected gravidas are identified as at risk of diabetes-related atherosclerosis, glomerular disruption, and pathogenic retinal angio-genesis. That GDM is evidence for underlying chronic conditions such as dysregulation of innate immune response that, independent of the diabetic state, produces vascular disease is difficult state, produces vascular disease is difficult to assert with the present published literature. Cross-sectional studies of patients with established gestational hypertension or preeclampsia are ambiguous as to the possible pathogenic effect of insulin resistance. Cohort studies initiated in early and mid-pregnancy show evidence that both gestational hypertension and preeclampsia may be more prevalent in gravidas with greater insulin resistance. The association of gestational glucose intolerance with gestational hypertension appears to be independent of obesity and ambient glycemia but explained in part by insulin resistance. Late pregnancy preeclampsia is associated with elevated mid-pregnancy BMI, blood pressure, fasting glucose and insulin, urate, and C-reactive protein, suggestive of metabolic and immune dysregulation. GDM appears to be associated with overexpressed innate immune response, which, in turn, is associated with vascular dysfunction and vascular disease. Among women with GDM, markers of insulin resistance do not appear to correlate with hypertension in short-term cohort studies. However, when non-GDM subjects are compared with subjects with GDM, postpregnancy studies do show an associated with vascular dysfunction and vascular disease. Among women with GDM, markers of insulin resistance do not appear to correlate with hypertension in short-term cohort studies. However, when non-GDM subjects are compared with subjects with GDM, postpregnancy studies do show an association of insulin resistance with both inflammatory dysregulation and vascular dysfunction. Cohort studies that have used population-based pregnancy databases consistently identify a clinically significant association of both gestational hypertension and preeclampsia with later hypertensive disorders. Associations with coronary artery disease or stroke are less consistent, requiring further investigation. Preventing the evolution of diabetes and lipid and immune dysregulation of the metabolic syndrome has become a silent public health issue because of the epidemic of childhood and early adulthood obesity and the opportunity at hand to treat insulin resistance by behavioral and pharmacological interventions. However, limited available literature highlights the need for long-term cohort studies of women with well-characterized metabolic and vascular profiles during pregnancy and decades later. Our present knowledge suggests that screening for GDM provides an opportunity of pregnancy outcome improvement. Limited studies of diabetes prevention in at-risk patient groups suggest that we may have the opportunity to reduce the risk of later diabetes. Additional investigation is required to determine if interventions that prevent or postpone diabetes also delay the onset of vascular disease.
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PMID:Gestational diabetes, pregnancy hypertension, and late vascular disease. 1759 80

The so-called epidemic of childhood obesity has increased the interest in the metabolic syndrome (MS) due to the potential projection into adulthood. Prevalence of the MS in adolescents has been estimated to be 6.7% in young adults and 4.2% in adolescents. Figures rise up to 28.7% in overweight and obese adolescents. The most widely accepted hypothesis links the syndrome to obesity. In the Bogalusa study, the best predictors were obesity and being in the upper quartile of basal insulin levels. Ethnic and genetic factors play a role in order to explain the syndrome in the non-obese population and the differences of interobesity. The relationship between MS and type 2 diabetes and cardiovascular disease is well established in adults. This association can be suggested in children as well, although the syndrome in childhood urgently needs to be clearly defined. In this age group, it is also of great interest to identify diagnosis criteria of the so-called pre-MS. Detection of the syndrome focuses mainly on obese and overweight young people. Other population groups such as newborns with low or high birth weight, infants with accelerated growth, or children of obese or with gestational diabetes mothers are at a higher risk of developing peripheral insulin resistance. The measurement of abdominal circumference can be a useful screening tool. Physical exercise and restriction of saturated and trans fatty acids are basic for treatment. If reducing weight is necessary, a reduction of carbohydrate intake, especially for refined sugars, must be emphasised. Dietary fibre improves insulin sensitivity.
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PMID:Metabolic syndrome in childhood. 1790 19

In utero hyperglycemia has been associated with insulin resistance (IR) in children; however, there are limited data in low-risk populations. The purpose of this study was to describe the prevalence of metabolic markers of IR in a primarily Caucasian cohort of gestational diabetes mellitus (GDM) offspring aged 7-11 yr (mean 9.1) and to correlate offspring with maternal indexes. Sixty-eight children were recruited through a follow-up study of women who participated in a randomized controlled trial of minimal intervention vs. tight glycemic control for GDM. All participants had a fasting plasma glucose (FPG), insulin, total cholesterol, high-density lipoprotein cholesterol (HDL-chol), triglyceride (TG) level, and a 2-h oral glucose tolerance test. We calculated homeostasis model assessment (HOMA) and recorded body mass index and waist circumference (WC). Criteria for metabolic syndrome for children included: FPG > 6.0 mmol/L, HDL-chol < 1.03 mmol/L, TG > 1.24 mmol/L, WC > 90% for age and gender, and 2-h glucose > 7.8 mmol/L. Among these children, 45 (66%), 17 (25%), 5 (7%), and 1 (1.5%) had zero, one, two, or three metabolic markers of IR, respectively. Hypertriglyceridemia (21%) was most prevalent, with no child having an elevated FPG. WC (p = 0.018) and TG (p = 0.005) were strong predictors of IR in the offspring after adjustment for age, gender, birthweight, family history, and maternal IR. Maternal and offspring HDL-chol, TG, WC, and HOMA but not fasting or 2-h glucose levels were significantly correlated. We conclude that metabolic markers of IR in children exposed to GDM may be present in the absence of abnormal fasting or 2-h glucose values. Screening strategies that focus on glucose levels may need to be reconsidered to institute early intervention with lifestyle changes for children at risk.
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PMID:Prevalence of metabolic markers of insulin resistance in offspring of gestational diabetes pregnancies. 1803 35

Physiological changes of pregnancy include insulin resistance and activation of the innate immunity with an inflammatory response. The working hypothesis is that the sub-clinical inflammation associated with excessive adiposity may favor the development of gestational diabetes (GDM) and Type 2 diabetes and other metabolic abnormalities related to cardiovascular disease later in life. In this paper we review the complex interrelationship among inflammatory markers, metabolic syndrome, and endothelium dysfunction in women with GDM and discuss if women with previous GDM (pGDM) could be considered at risk for cardiovascular diseases. MEDLINE was searched for articles relating GDM and the adipokines (tumor necrosis factor-alpha and adiponectin) as well as the acute-phase inflammatory biomarker C-reactive protein that contribute to the development of diabetic pregnancy and vascular complications. However, to date, in pGDM women no prospective study is available, to corroborate the hypothesis that inflammatory pattern could be taken as predictor of cardiovascular disease later in life. Therefore, our paper should provide arguments to perform follow-up programs to prevent cardiovascular events in women with pGDM. Control of body weight, regular physical exercise are indeed powerful intervention tools able at improving insulin sensitivity and reduce sub-clinical inflammation, both involved in the pathogenesis of cardiovascular disease.
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PMID:Gestational diabetes, inflammation, and late vascular disease. 1807 92

The recognition that insulin resistance has a pivotal role in the pathogenesis of polycystic ovary syndrome (PCOS) revolutionized our understanding of this complex disorder. PCOS causes major metabolic and reproductive morbidities, including substantially increased risk for type 2 diabetes mellitus and the metabolic syndrome. Insulin-sensitizing drugs (ISDs) ameliorate reproductive abnormalities, restore ovulation and regular menses, increase pregnancy rates and reduce androgenic symptoms in affected women with PCOS. Accordingly, ISDs, specifically metformin, have been widely adopted as therapy for this condition. A recent, large, randomized, multicenter, clinical trial that assessed live-birth rates rather than surrogate end points suggested that metformin alone is inferior to clomiphene citrate in treating infertility associated with PCOS. There is, furthermore, no evidence to support the use of metformin during pregnancy to prevent spontaneous abortions or gestational diabetes mellitus in women with PCOS. Renewed safety concerns about thiazolidinediones followed recent studies that reported increased cardiovascular morbidity with these agents. These concerns might preclude thiazolidinedione use in otherwise healthy women with PCOS. Finally, although ISDs improve insulin action and cardiovascular disease risk, there is no evidence that they provide long-term health benefits in PCOS. This article discusses the role of ISDs in PCOS in light of these new data.
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PMID:Drug insight: insulin-sensitizing drugs in the treatment of polycystic ovary syndrome--a reappraisal. 1836 5


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