The Metabolic Syndrome: Epidemiology Clinical Treatment and Underlying Mechanisms
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There are currently several ongoing prospective and randomized studies attempting to prevent oxidative stress during gestation. In pregnancies where uterine growth is restricted, there is increased placental vascular resistance, which in turn increases afterload on the fetal heart, which may impact on fetal programming for cardiovascular disease. A deficiency in the action of the placental enzyme 11 b HSD 2 hydroxysteroid dehydrogenase type 2 provokes increased exposure to maternal cortisol, which may program the fetus for arterial hypertension and metabolic diseases.
The placenta functions as a sensor of nutritional status, regulating nutrient transport in accordance with supply. This is why the placenta plays a fundamental role in fetal programming. Changes to the maternal compartment can cause mitigation of placental genes, increasing oxidative stress and modifying placental function. Newborn infants subjected to a hyperinsulinemic uterine environment also exhibit an increased risk of developing metabolic syndrome in adulthood. Boney et al. The study followed-up 84 children in the LGA group and 95 in the AGA group, at ages 6, 7, 9 and 11 years, the mothers of whom did or did not have a history of gestational diabetes.
The Metabolic Syndrome:
Anthropometric and biometric measurements were taken at 6, 7, 9 and 11 years. The status of LGA and maternal obesity, individually, doubled the risk of developing metabolic syndrome. More recently, some authors hypothesize that one important determinant of the emergence of metabolic syndrome in adulthood is rapid weight gain, especially fat, during the postnatal period, which is very common among SGAs with catch-up growth.
From this fact it can be concluded that the Barker hypothesis could be applied to the postnatal period. Accumulation of adipose tissues, particularly in the abdominal region, is fundamental to triggering off the metabolic syndrome. There is an association between adipose tissue and the principal inflammatory cells, leading to an increase in production of inflammatory mediators and increased liberation of free fatty acids, the effects of which are felt both in the Langerhans beta islet cells and their receptors and also in the vascular wall. Studies with children and adolescents have confirmed that these phenomena begin early on.
Metabolic syndrome in the pediatric age group. According to the NCEP diagnostic criteria, the prevalence of metabolic syndrome among American adults was 6. Insulin resistance is the pathophysiologic basis for the emergence of the metabolic syndrome. Some prospective studies, like the Cardiovascular Risk in Young Finns Study and the Bogalusa Heart Study have demonstrated that hyperinsulinemia and, in particular, childhood obesity, are risk factors for the metabolic syndrome and that early hyperinsulinemia precedes the emergence of the metabolic syndrome, even in childhood.
Childhood obesity, defined as a BMI greater than the 95th percentile for age, after 3 years, exhibits an important association with obesity in adulthood, and its prevalence has tripled over the last 3 decades. Insulin resistance can be assessed in a variety of ways and, in clinical practice, insulinemia and the HOMA index homeostasis model assessment are widely used.
However, these methods have not yet been standardized for children and adolescents. Tresaco et al. Glucose intolerance and insulin resistance are often found among obese children and adolescents. The individuals who are at greatest risk of developing diabetes mellitus type 2 those who are obese and those who have acanthosis nigricans and a family history. In general, after ten years of age, adolescents develop this type of diabetes, possibly because the hormonal changes of puberty contribute to exacerbation of the disease.
Sinha et al.
The Metabolic Syndrome:
Studies like the Bogalusa Heart Study and the Muscatine Study have demonstrated that obesity in adolescents is correlated with a proatherogenic dyslipidemic profile, with increased LDL cholesterol, potentiating the cardiovascular risk, itself already elevated due to the obesity. Weight loss has a major impact on the metabolic syndrome.
Changes aimed at achieving healthy diet must be embarked on by the entire family, with the intention of increasing the consumption of fruit, vegetables, skimmed milk products and water, two fraction feeding and reduce consumption of fried food, pastries, sweets and processed meat products. Promotion of physical activity, whether programmed or not, reducing the child's idle time, especially in front of the television and computer, is another crucial point.
The entire family should also be involved in this process.
In pediatrics, pharmacological treatment of obesity should be restricted to cases that are most resistant to clinical treatment and of the greatest severity. In the United States, only sibutramine and orlistat have been approved, for use with children over 12 years of age. Metformin is indicated for children with glucose intolerance or diabetes mellitus type 2.
In these patients the drug has an anorexigenic effect, reducing glucose and insulin levels and improving the lipid profile. Hypertension and dyslipidemia should also be treated with lifestyle changes and drugs, depending on the severity of the case. Bariatric surgery for the treatment of adolescent obesity is an extremely invasive procedure and it can only be indicated in extremely restricted circumstances in this age group. The American Pediatric Surgical Association Clinical Task Force on Bariatric Surgery recommends that adolescents may be candidates for the procedure if they have a BMI greater than 50, or greater than 40 and associated with comorbidities sleep apnea, diabetes mellitus type 2 , are at a minimum Tanner puberty stage of III, a multidisciplinary team has failed to achieve a response after at least 6 months' treatment, medical and psychological assessments have been completed, there are severe problems socializing, there is good family support and if they are over 13 years old and have the capacity to take informed decisions.
In summary, treatment and prevention of childhood obesity have become a public health priority. Acquisition of excessive fat during the postnatal period is related to insulin resistance in adulthood and breastfeeding may prevent this obesity. Ceballos LT. An Pediatr Barc. Reaven GM. Banting lecture Role of insulin resistance in human disease. Prevalence of a metabolic syndrome phenotypes in adolescents: findings from the third National Health and Nutrition Examination Survey, Arch Pediatr Adolesc Med. Evaluation of waist circumference, waist-to-hip ratio, and the conicity index as screening tools for high trunk fat mass, as measured by dual-energy X-ray absorptiometry, in children aged y.
Am J Clin Nutr. World Health Organization. World Health Statistics Geneva: WHO; International statistical classification of diseases and related health problems.
Endocrine regulation of human fetal growth: the role of the mother, placenta, and fetus. Endocr Rev. Bursztyn M, Ariel I.
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Maternal-fetal deprivation and the cardiometabolic syndrome. J Cardiometab Syndr. Mechanisms by which poor early growth programs type-2 diabetes, obesity and the metabolic syndrome. Physiol Behav. Type 2 non-insulin-dependent diabetes mellitus, hypertension and hyperlipidaemia syndrome X : relation to reduced fetal growth. Neel JV. Diabetes mellitus: a "thrifty" genotype rendered detrimental by "progress"? Am J Hum Genet. Although ATP III identified cardiovascular disease CVD as the primary clinical outcome of the metabolic syndrome, we now have evidence that metabolic syndrome is associated with type 2 diabetes mellitus, polycystic ovarian disease, nonalcoholic fatty liver disease, and possibly some cancers.
This review summarizes evidence in support of the relationship between metabolic syndrome and various cancers and possible underlying mechanisms and therapeutic interventions. Login to your account Username.kessai-payment.com/hukusyuu/geolocalisation/ge-logiciel-espion.php
Metabolic syndrome: identifying the risk factors
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Metabolic Syndrome and Related Disorders Vol. Pooja PothiwalaM. Sushil K. Subhashini YaturuM. Obesity is a predictor in prostate cancer patients receiving prostatectomy after neoadjuvant hormonal therapy. CNS-targeting pharmacological interventions for the metabolic syndrome. Pathobiological mechanisms underlying metabolic syndrome MetS in chronic obstructive pulmonary disease COPD : clinical significance and therapeutic strategies. Association between diabetes and oncological outcomes in patients undergoing neoadjuvant chemo-radiotherapy for rectal cancer.
Prediction of the development of metabolic syndrome by the Markov model based on a longitudinal study in Dalian City. Neuroendocrine and immune disequilibrium as a probable link between metabolic syndrome and carcinogenesis. Characterization and prevalence of metabolic syndrome among overweight and obese young Palestinian students at An-Najah National University. The prevalence trend of metabolic syndrome and its components and risk factors in Korean adults: results from the Korean National Health and Nutrition Examination Survey — Case-control study of metabolic syndrome and ovarian cancer in Chinese population.
Circulating bone morphogenetic protein-9 in relation to metabolic syndrome and insulin resistance. Thyroid disorders in obese patients. Does insulin resistance make a difference? Nutritional and Acquired Deficiencies in Inositol Bioavailability. Correlations with Metabolic Disorders.