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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polycystic ovary syndrome (PCOS) is the commonest endocrine disturbance affecting women. There is considerable heterogeneity of symptoms and signs amongst women with PCOS and for an individual these may change over time. PCOS is familial and genetics appear to be associated with disturbances of insulin secretion. Polycystic ovaries can exist without clinical signs of the syndrome, which may then become expressed over time. There are a number of interlinking factors that affect expression of PCOS. A gain in weight is associated with a worsening of symptoms whilst weight loss will ameliorate the endocrine and metabolic profile and symptomatology. Women with PCOS are characterized by the presence of insulin resistance, central obesity and dyslipidaemia, which appears to place them at a higher risk of developing diabetes as well as cardiovascular disease. A number of studies have confirmed the higher incidence of diabetes, although they have not shown a higher risk of mortality from ischaemic heart disease (IHD). Cross-sectional studies have demonstrated a significant association between PCOS and IHD. Prospective, long-term longitudinal studies confirming this risk are still awaited. Weight loss remains the most effective first line therapeutic intervention in women with PCOS and recently the use of insulin sensitizing agents has demonstrated benefit.
Best Pract Res Clin Obstet Gynaecol 2003 Apr
PMID:Polycystic ovary syndrome--a systemic disorder? 1275 99

This chapter provides background on the nutritional health of adolescents, focusing on a public health or population-level approach. We detail some specific nutritional issues and related health outcomes that are particularly relevant to adolescents, including overweight and obesity, type 2 diabetes, eating-related disorders and bone health as it relates to calcium intake. We discuss implications of the trends in adolescent dietary habits for practitioners and propose a research agenda for better understanding and positively influencing future adolescent nutritional health.
Best Pract Res Clin Endocrinol Metab 2003 Jun
PMID:Nutritional issues for adolescents. 1278 46

Obesity is commonly associated with elevated plasma levels of free fatty acids (FFAs). High levels of FFA have emerged as a major link between obesity and insulin resistance/type 2 diabetes (T2DM). Thus, acute and chronic elevations of plasma FFAs produce insulin resistance in skeletal muscle and liver. In skeletal muscle, FFA-induced insulin resistance is associated with accumulation of intramyocellular triglyceride and diacylglycerol, and with activation of protein kinase C (the beta and delta isoforms). It is suggested that FFAs interfere with insulin signalling via PKC-induced serine phosphorylation of the insulin receptor substrate-1. In the liver, FFAs cause insulin resistance by interfering with insulin suppression of glycogenolysis. In beta-cells, FFAs potentiate glucose-stimulated insulin secretion acutely and chronically. It is postulated that this prevents the development of T2DM in most (>80%) obese insulin-resistant people who have FFA-mediated insulin resistance. Elevated levels of FFA also seem to activate a pro-inflammatory and pro-atherogenic pathway (the IkappaB/NFkappaB pathway) and may be responsible, at least in part, for the increase in atherosclerotic vascular disease seen in patients with T2DM. As increased plasma levels account for up to 50% of insulin resistance in obese patients with T2DM, lowering of plasma FFAs could be a new and promising approach to the treatment of T2DM.
Best Pract Res Clin Endocrinol Metab 2003 Sep
PMID:Nutritional effects of fat on carbohydrate metabolism. 1296 93

Based on our investigations in first-degree relatives, in twins in general, and in monozygotic twins discordant for type 2 diabetes, we have studied the inheritance of glucose intolerance, insulin resistance and insulin secretion in order to evaluate the role of genes versus environment in the development of type 2 diabetes. Insulin resistance in type 2 diabetes is mainly linked to glucose disposal in skeletal muscle, i.e. reduced glycogen synthesis. In order to investigate the genetic component responsible for the reduced glycogen synthase activity and reduced glucose transport, we also investigated cultured myotubes based on in vivo skeletal muscle biopsies. The results obtained in our own studies are discussed in comparison with the international literature. We conclude that both genetic and environmental factors play a role in the development of type 2 diabetes (hyperglycaemia), and that only subjects who are genetically disposed to insulin resistance and who possess beta-cells which are unable to compensate for the degree of insulin resistance seem to develop type 2 diabetes. Variables of two gene alleles disposing to insulin resistance have been identified, and their role is discussed. The most important environmental factor seems to be obesity, but intrauterine malnutrition also plays a role. The cellular mechanism responsible for obesity/lipid-induced diabetes mellitus is discussed with specific emphasis on the role of accumulation of long-chain AcylCoA and triglycerides in liver, muscle and beta-cells.
Best Pract Res Clin Endocrinol Metab 2003 Sep
PMID:Metabolic and genetic influence on glucose metabolism in type 2 diabetic subjects--experiences from relatives and twin studies. 1296 96

Hyperuricemia (HU) is present in 5-30% of the general population, although the prevalence is higher among some ethnic groups and seems to be increasing worldwide. Classically, chronic HU has been considered a risk factor for gout or lithiasis and is associated with alcoholism, obesity, hypertension, dyslipidemia, hyperglycemia/diabetes mellitus, renal failure and intake of certain drugs. HU is also associated with cardiovascular diseases such as hypertension, vascular disease, pre-eclampsia, pulmonary arterial hypertension, stroke, heart failure, ischemic heart disease and also metabolic syndrome, renal disease and increased mortality. It is uncertain if these associations are dependent or not, especially cardiovascular and renal diseases. Patients with chronic HU and also those with gout require both medical investigation for associated diseases or drugs as well as nutritional counseling and life-style changes. HU should alert physicians to possible complications.
Best Pract Res Clin Rheumatol 2004 Apr
PMID:Primary prevention in rheumatology: the importance of hyperuricemia. 1512 Oct 34

The purpose of this study was to determine the relationship between BMD and childhood obesity. We examined 1070 obese children (722 boys and 348 girls) aged 7 to 15 years. Their mean relative weight, as a percentage of the standard weight for age, height, and sex, was 152.9 +/- 14%. BMD was assessed, by a digital image processing method, in the second metacarpal bone of the left hand. We compared our results with those of healthy nonobese Japanese children based on both chronological and bone age. Mean BMD values for bone age in the obese children were significantly higher than those in control groups in boys aged 11 years and under and girls 9 years and under. On the other hand, in boys over 12 years old, BMD values for bone age were lower than those in the control groups. In girls over 11 years old, BMD values tended to be lower than those in the control groups. In conclusion, we studied the BMD of obese children from the point of view of advanced bone age. Our results showed that BMD was higher than in prepubertal obese children, but a low BMD value was found after puberty, due to poor gain of BMD during puberty. It is important to prevent obesity in childhood in order to prevent the low BMD after puberty.
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PMID:Obese Japanese children have low bone mineral density after puberty. 1522 98

Leptin is a hormone involved with satiety and energy balance and proposed to be an anti-obesity factor. Much effort has been dedicated to the relationship between leptin and bone. This interest stems from the knowledge that body weight is a major determinant of bone density. It is known that obese persons have stronger bones and lose bone tissue at a slower pace. Therefore, attention has been given to leptin as a mediator of increased osteogenesis. Leptin has been shown to play a role on bone both in vitro and in vivo. The administration of leptin in vitro induced the expression of leptin receptors on stromal cells, the differentiation to osteoblasts and inhibition of differentiation into the adipocyte phenotype. In addition, leptin was able to inhibit osteoclastogenesis of peripheral blood mononuclear cells. Therefore, there is in vitro and experimental evidence that leptin is able both to stimulate osteoblasts and inhibit osteoclast differentiation. This would be in line with the hypothesis that the correlation between obesity and increased BMD is linked to leptin activity. However, experimental results are indicative of a role of CNS in mediating the effect of leptin on bone metabolism. These effects are opposite to the direct effects on bone cells and lead to bone loss. To solve the problem, it has been suggested that obese individuals have a resistance of nervous structures to leptin. In chronic renal failure serum leptin levels are markedly increased. An inverse correlation between histomorphometric parameters of bone turnover and serum leptin levels and between leptin and PTH have been reported. Therefore, the hypothesis has been raised that leptin lowers bone turnover in chronic renal failure. Since leptin has a direct stimulatory effect on bone and an indirect opposite effect via the CNS, it has been suggested that in CRF a resistance of nervous structures to leptin, like in obesity, may be present. By now, coherent findings suggest that the prevailing effect of leptin on bone in ESRD is that of reducing bone turnover.
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PMID:Leptin and bone metabolism. 1529 17

Polycystic ovarian morphology is seen on ultrasound in approximately 22% of women. Polycystic ovary syndrome (PCOS) is a common and perplexing endocrine disorder of women in their reproductive years, with a prevalence of up to 10%. Clinical expression of the syndrome varies but commonly includes menstrual cycle disturbance, hyperandrogenism, insulin resistance and obesity. Recently, the European Society for Human Reproduction and Embryology and the American Society for Reproductive Medicine (ESHRE/ASRM) achieved a new consensus regarding the definition of PCOS. This is now defined as the presence of any two of the following three criteria: (i) polycystic ovaries; (ii) oligo-/anovulation; and/or (iii) clinical or biochemical evidence of hyperandrogenism. This revised definition provides an international framework for the clinical assessment of PCOS and for future research and collaboration.
Best Pract Res Clin Obstet Gynaecol 2004 Oct
PMID:Definitions, prevalence and symptoms of polycystic ovaries and polycystic ovary syndrome. 1538 Jan 40

Polycystic ovary syndrome (PCOS) is a common clinical and metabolic condition in women of reproductive age. It is associated with short-term reproductive and long-term metabolic dysfunction. Treatment has traditionally focused on fertility and hormonal therapy. However, general obesity, central obesity and insulin resistance are strongly implicated in its aetiology and improving these factors has proved highly successful in some clinical situations, reducing the need for costly assisted reproduction. A low-fat, high-carbohydrate diet is thought to improve insulin sensitivity, aid in weight loss and reduction of metabolic and reproductive symptoms and improve the long-term maintenance of a reduced weight. However, there has been recent community interest in adopting a protocol advocating a moderate increase in dietary protein for improving weight loss and PCOS symptoms. Altering the glycaemic index of the diet has also received considerable attention as a regime for promoting satiety and reducing metabolic risk factors for type 2 diabetes mellitus and cardiovascular disease. Exercise and other lifestyle changes are essential for altering the short- and long-term effects of PCOS. It is vital that the efficacy of these strategies is assessed so that accurate medical and dietetic advice can be given both to patients and to the health-care community.
Best Pract Res Clin Obstet Gynaecol 2004 Oct
PMID:Understanding and managing disturbances in insulin metabolism and body weight in women with polycystic ovary syndrome. 1538 Jan 43

Women with polycystic ovary syndrome (PCOS) frequently present with reproductive dysfunction. Ovarian function might be disturbed, with resultant abnormal folliculogenesis and steroidogenesis and, although it is difficult to define the exact pathogenesis of anovulation, many possible mechanisms have been postulated. Folliculogenesis in anovulatory women with PCOS is characterized by failure of dominance and the ovary has multiple small follicles, which are arrested but capable of steroidogenesis. Abnormalities in gonadotrophin and insulin secretion and disordered paracrine function have been identified. Women with PCOS have an increased prevalence of miscarriage, both after spontaneous and induced ovulation. Hypersecretion of LH, hyperandrogenaemia and hyperinsulinaemia have all been investigated as possible causes of PCOS. It is likely that these factors are interlinked and together might result in disordered ovarian and endometrial function. Multiple other possible abnormalities have been postulated as contributory factors in the reproductive failure. These include decreased plasminogen activator inhibitor activity, endothelial dysfunction and obesity. Ideally, therapy should target the underlying disorders but at present data are inadequate and further investigations are essential before therapeutic recommendations are truly based on an understanding of the pathophysiology.
Best Pract Res Clin Obstet Gynaecol 2004 Oct
PMID:The pathogenesis of infertility and early pregnancy loss in polycystic ovary syndrome. 1538 Jan 45


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