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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 presence of insulin-dependent or non insulin-dependent diabetes mellitus in pregnant women has been associated with an adverse effect on the maternal an fetal outcomes of pregnancy. The incidence of obstetrical and diabetic complications is increased, and a continuum has been observed between maternal blood glucose levels and perinatal outcome. The incidence of congenital malformations, macrosomia and prematurity is increased in offspring of diabetic mothers. Programming and intensive collaborative follow-up improve the outcome of such pregnancies. Gestational diabetes mellitus is an heterogenous condition defined as carbohydrate intolerance of variable severity with onset or first recognition during pregnancy. Short term complications are mainly represented by fetal macrosomia and high cesarean section rate. Women with a history of gestational diabetes mellitus are at increased risk of future diabetes, predominantly type 2. Obesity and type 2 diabetes are increased among their children.
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PMID:[Diabetes and pregnancy]. 1054 52

Evidence has accumulated that small for gestational age (SGA) children have long-term adult health consequences including obesity, Type 2 diabetes mellitus, hypertension, coronary artery disease and stroke. This increased risk of later adult disease is likely a consequence of an early, persistent reduction in insulin sensitivity. The SGA children and adults studied were predominantly at term gestation, and it appears that prematurity also leads to insulin resistance with possibly similar health consequences for later life. Both term SGA and premature children have an abnormal early environment: one in utero and one post-natally. Parallels are made among those born SGA at term or premature to show the potential importance of maternal factors, the intrauterine milieu, including nutrient supply and intake in fetal and early newborn life. It is possible that manipulation of these factors during early neonatal life in premature babies could lead to normalisation of insulin sensitivity. To confirm this hypothesis, further studies are needed to better understand the pathophysiological mechanisms leading to reduced insulin sensitivity and confirm that prematurity is linked with similar long-term health consequences as being born SGA.
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PMID:Insulin sensitivity in people born pre-term, with low or very low birth weight and small for gestational age. 1661 99

IR is hypothesized to be the important pathophysiologic link between adiposity and future development of type 2 diabetes and cardiovascular disease. A variety of methods for measuring IR have been validated in children, from the gold-standard hyperinsulinemic euglycemic clamp, to simple fasting measures based on fasting insulin and glucose levels. Studies have shown that there are a number of important risk factors for IR in children, including adiposity and visceral adiposity, race/ethnicity, puberty, a family history of type 2 diabetes, sex, and being small for gestational age or prematurity. However, obesity represents the critical risk factor for IR in children. Greater than 50% of obese adolescents in the US have IR. Formal assessment of IR in obese children may represent an important strategy for improving the efficacy of pharmacologic therapy for weight loss and chronic disease prevention.
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PMID:Insulin resistance in children and adolescents. 1716 45

Genetic and environmental factors influence insulin sensitivity (IS) during one's lifetime. Actually, uterine environment may affect IS at birth and later in life. In particular, various exogenous toxic substances, coupled to a genetic predisposition, may remarkably influence the regulation of the hypothalamus-hypophysis-adrenal gland axis, and the production or the activity of insulin, cerebral incretins, pro-inflammatory cytokines, and placental hormones. Owing to this reaction against environmental injuries, fetal growth and endocrine system development may be impaired, leading to low or large birth weight, or prematurity. Reduced growth in early life has been related to insulin resistance, which can be silent for years and evident in predisposed adults. The incidence of type 2 diabetes mellitus and obesity associated with sedentary lifestyle patterns and inadequate dieting behaviors in children and adolescents has rapidly increased during the last decade. Recent evidences suggest that the Pro12Ala polymorphism of the peroxisome proliferator-activated receptor- (PPAR-) gene and the angiotensin converting enzyme (ACE) I/D gene polymorphism combined with environmental factors, such as phthalates interfering with the post receptorial action of insulin, alter insulin-sensible tissues. Therefore, IS, deriving from a complex interaction between genotype and environment, may change during life and depends on previous metabolic control, which is a sort of metabolicmemory. The goal for the future is preventing the complications associated with impaired IS through the control of exogenous factors and the use of drugs selectively effective on its pathogenesis.
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PMID:Influence of environment on insulin sensitivity. 1939 33

Intrauterine Growth Retardation (IUGR) is defined as a rate of growth of a fetus that is less than normal for the growth potential of the fetus (for that particular gestational age). Small for Gestational Age (SGA) is defined infant born following IUGR, with a weight at birth below the 10th percentile.Suboptimal fetal growth occurring in IUGR fetuses is an important cause of perinatal mortality and morbidity. The acute neonatal consequences of IUGR include metabolic and hematological disturbances, and disrupted thermoregulation; in addition, respiratory distress (RDS), necrotizing enterocolitis (NEC), and retinopathy of prematurity (ROP) may contribute to perinatal morbidity. Metabolic disturbances are related to glucose and fatty acid metabolism. It is well-known that individuals who display poor growth in utero are at significantly increased risk for type 2 diabetes mellitus (T2DM), obesity, hypertension, dyslipidemia, and insulin resistance (the so-called metabolic syndrome, MS). MS ultimately leads to the premature development of cardiovascular diseases. In addition, short stature in children and adults, premature adrenarche, and the polycystic ovarian syndrome (PCOS) are endocrinological sequelae of IUGR. (8) Early onset growth delay and prematurity significantly increase the risk for neurological sequelae and motor and cognitive delay.Future prospective studies need to investigate risk factors for infants who are SGA. If reliable prediction can be achieved, there is potential to reduce future perinatal morbidity and mortality, and long term consequences among SGA babies.
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PMID:Short-term and long-term sequelae in intrauterine growth retardation (IUGR). 2303 Jul 65

Low birth weight is related to increased risk of developing cardiovascular disease and type 2 diabetes in adult life. Since obesity is closely associated with type 2 diabetes and cardiovascular disease, the relationship between size at birth and adult anthropometry is of interest as a mediator of the relationship between birth weight and metabolic diseases. The aim of this study was, therefore, to examine the effect of size at birth and prematurity on measures of adult anthropometry taking adult socio-economic status and lifestyle variables into account. Midwife records with information on mother's age and parity as well as weight, length and maturity at birth were traced in 4744 Danes born between 1939 and 1970. Measures of adult anthropometry (weight, height, body mass index (BMI), waist circumference, hip circumference and waist/hip ratio) had previously been recorded together with information on socio-economic factors, lifestyle and parental diabetes status. Mother's age, parity and diabetes status were associated with offspring birth weight. Size at birth was positively associated with adult height and weight, but only weakly associated with BMI and not associated with waist/hip ratio when adjusted for socio-economic and lifestyle factors. Infants born preterm were less growth restricted at birth and grew to be taller and heavier compared with term infants born small for gestational age. Altogether, this study does not find evidence that obesity or a central fat distribution is mediating the relationship between low birth weight and risk of cardiovascular disease or type 2 diabetes in later life.
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PMID:Impact of size at birth and prematurity on adult anthropometry in 4744 middle-aged Danes - The Inter99 study. 2514 35

Overweight during pregnancy predisposes both the mother and foetus to health complications. Maternal complications include gestational diabetes, obstetric problems and type 2 diabetes later in life. Complications for the offspring are not only restricted to the foetal period or birth, such as prematurity and foetal macrosomia, but may also have long-term metabolic health implications through the mechanism of early nutrition programming. One of the key metabolic components characterising overweight in the non-pregnant state is low-grade inflammation manifested by elevated levels of circulatory pro-inflammatory cytokines. In pregnancy, in addition to adipose tissue and placenta, inflammatory response may originate from the gut. The extent to which overweight induces metabolic maladaptation during pregnancy and further compromises maternal and child health is currently poorly understood. In this review, we evaluate recent scientific literature and describe the suggested links between overweight, gut and low-grade inflammation associated metabolic disorders. We focus on overweight pregnant women and gestational diabetes, and discuss how specific dietary factors, probiotics and long-chain polyunsaturated fatty acids (fish oil), might confer health benefits in combatting against metabolic risk factors.
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PMID:Opportunities for probiotics and polyunsaturated fatty acids to improve metabolic health of overweight pregnant women. 2793 67

Intrauterine growth restriction (IUGR) is when fetuses and newborn infants have not reached their true growth potential as genetically defined. Fetuses with IUGR develop in a less than ideal environment that leads to epigenetic changes and marks infants' metabolism for the rest of their lives. Epigenetic changes affect insulin-like growth factor-1 (IGF-1) levels and lead to insulin resistance and ultimately to a metabolic syndrome. The metabolic syndrome is a constellation of illnesses that raise one's risk for type 2 diabetes mellitus, coronary artery disease, and ischemic heart disease, including hypertension, dyslipidemia, central obesity, insulin resistance, and inflammation. The association between IUGR or prematurity and long-term insulin resistance, obesity, hypertension, and metabolic syndrome remains unclear. While studies have shown an association, others have not supported such association. If alteration of intrauterine growth can ultimately lead to the development of metabolic derangements in childhood and adulthood, and if such association is true, then early interventions targeting the health of pregnant women will ensure the health of the population to follow.
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PMID:Prevalence of diabetes and obesity in association with prematurity and growth restriction. 2874 Apr 12

Premature birth affects more than 10% of live births, and is characterized by relative hyperoxia exposure in an immature host. Long-term consequences of preterm birth include decreased aerobic capacity, decreased muscular strength and endurance, and increased prevalence of metabolic diseases such as type 2 diabetes mellitus. Postnatal hyperoxia exposure in rodents is a well-established model of chronic lung disease of prematurity, and also recapitulates the pulmonary vascular, cardiovascular, and renal phenotype of premature birth. The objective of this study was to evaluate whether postnatal hyperoxia exposure in rats could recapitulate the skeletal and metabolic phenotype of premature birth, and to characterize the subcellular metabolic changes associated with postnatal hyperoxia exposure, with a secondary aim to evaluate sex differences in this model. Compared to control rats, male rats exposed to 14 days of postnatal hyperoxia then aged to 1 year demonstrated higher skeletal muscle fatigability, lower muscle mitochondrial oxidative capacity, more mitochondrial damage, and higher glycolytic enzyme expression. These differences were not present in female rats with the same postnatal hyperoxia exposure. This study demonstrates detrimental mitochondrial and muscular outcomes in the adult male rat exposed to postnatal hyperoxia. Given that young adults born premature also demonstrate skeletal muscle dysfunction, future studies are merited to determine whether this dysfunction as well as reduced aerobic capacity is due to reduced mitochondrial oxidative capacity and metabolic dysfunction.
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PMID:Sex-Specific Skeletal Muscle Fatigability and Decreased Mitochondrial Oxidative Capacity in Adult Rats Exposed to Postnatal Hyperoxia. 2965 Dec 55

There are in France several millions of shift-workers and night-workers (20 to 25% of employees). These workers are therefore subject to variations in their working and rest schedules. These regular schedule changes are associated with repeated desynchronization of circadian biological clock. The negative impacts on sleep are insomnia, drowsiness, and reduced sleep time in 24hours. There is also a proven effect on the occurrence of a metabolic syndrome, with a likely effect on obesity, type 2 diabetes, blood pressure and coronary artery disease. There is a likely effect on the occurrence of cancer (including breast cancer). Night working is not recommended for pregnant women because of the risk of miscarriage, prematurity and intrauterine growth retardation.
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PMID:[Shift-workers and night-workers' health consequences: State of art and recommendations]. 3044 36


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