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

Over the last decade growing evidence has been documented on the relationship between intrauterine growth retardation (IUGR) and pubertal development indicating changes in timing and progression of puberty. These changes in pubertal development are part of a growing list of IUGR-related diseases, which includes type 2 diabetes mellitus, cardiovascular disease, short stature and polycystic ovary syndrome. The influence of IUGR on the mechanisms behind the onset of puberty is still elusive. In the absence of prospective studies on gonadotropin-releasing hormone pulse patterns in IUGR children, other markers of pubertal development such as age at menarche in girls and progression of puberty have been employed. We investigated pubertal development and DHEAS levels in children born small for gestational age (SGA) after third trimester growth retardation and children born appropriate for gestational age (AGA). A faster progression of puberty was found in girls but not in boys. DHEAS levels tended to be higher in SGA children than in AGA children. In animal studies using two rat models, growth and onset of puberty based on perinatal undernutrition were also investigated. In one model intrauterine growth retardation was induced by ligation of the uterine arteries (IUGR) at day 17 of gestation and in the other model postnatal food restriction (FR) was induced by increasing litter size after birth until weaning. In both models, the rats showed a persistent growth failure. Onset of puberty was defined by vaginal opening (VO) in female rats and by balanopreputial separation (BPS) in male rats. At onset of puberty IUGR and FR rats had a lower body weight compared to controls, indicating that no threshold for body weight is needed for the onset of puberty. In the IUGR female rats, the onset of puberty was delayed and in the FR female rats the onset of puberty was in time. In both IUGR and FR female rats VO and first cycle were uncoupled. In IUGR female rats, at VO, at first cycle and at the age of 6 months the ovaries showed a decline in number of follicles indicating that intrauterine malnutrition in the female rat has a permanent influence on the growth and development of follicles. In the FR female rats, at VO, the ovaries showed a normal number of follicles but an abnormal maturation pattern. At the time of first cycle and at the age of 6 months normalization in follicle growth pattern was observed. These findings suggest that postnatal undernutrition has a transient influence on follicle growth and development. In male rats, both models showed delayed onset of puberty and impaired testicular function, as shown by decreased testosterone levels. These data indicate that early malnutrition during different critical developmental time windows may result in different long-lasting effects on pubertal development in both humans and rats.
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PMID:Fetal nutrition and timing of puberty. 1572 15

The metabolic syndrome has several similarities with Cushing's syndrome (impaired glucose tolerance, hypertension, dyslipidemia, central obesity) suggesting that abnormalities in the regulation of the hypothalamic-pituitary-adrenal axis may have a link with the metabolic syndrome. Several studies suggested an association between the clinical signs of the metabolic syndrome and the increased hypothalamic-pituitary-adrenal axis activity based on increased cortisol concentration at 09.00 a.m. and increased cortisol response to corticotropin. According to the Barker hypothesis the fetal malnutrition could determine adult cardiovascular diseases (coronary heart disease, hypertension), some endocrine and metabolic disorders (obesity, type 2 diabetes and hyperlipidemia). The suggested mechanism of the phenomenon is that the suboptimal fetal nutrition results in glucocorticoid overproduction. The 11beta-hydroxysteroid dehydrogenase (converts biological inactive cortisone to cortisol and vice versa) is an important enzyme in cortisol metabolism. The increased expression of 11beta-hydroxysteroid dehydrogenase type 1 in fat tissue could lead to central obesity and impaired glucose tolerance. The hypothesis that increased corticotropin-releasing hormone production drives the overactive hypothalamo-pituitary-adrenal axis was not proven. Further investigations are needed to identify additional pathogenetic factors and to find new therapeutic possibilities.
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PMID:[Correlations between the hypothalamo-pituitary-adrenal axis and the metabolic syndrome]. 1572 52

Iodine prophylaxis in Poland started in 1997 and is based on mandatory iodzation of household salt with 20-40 mg KI/ 1 kg, supplementation of bottle fed infants with iodized formulas with 10,0 microg KI/100 ml, and a voluntary supplementation of pregnant and breast feeding women with additional 100-150 microg of iodine/ day. Last evaluation of efficacy of the iodine prophylaxis performed in 2003 by WHO and International Council for the Control of Iodine Deficiency Disorders allocated Poland within the group of the European countries with sufficient iodine supplementation on the population level. However according to data of the Institute of Mather and Chield in Poland, around 50 % of pregnant women only is additionally supplemented with iodine. Iodine deficiency during pregnancy even as a moderate iodine deficiency, creates a risk of mental retardation, perinatal complication like low and very low births weigt of neonates with increased perinatal mortality rate and late consequences in adult life: metabolic syndrom and type 2 diabetes. Another limitation of the actual model of iodine prophylaxis in Poland, it is too high consumption of natrum chloride (over 5,0 g of household salt/day/ capita). It is around 50% over WHO recommendation. Intensive preventive program against hypertension, type 2 diabetes, atherosclerosis, osteoporosis and some neoplasmatic diseases includes limitation of natrum chloride consumption- as one of the risk factors. Therefore new scope of the National Programme for Elimination of Iodine Deficiency will include: a special prorgramme for the iodization of animal food according to european standard, increased rate of pregnant women additionally supplemented with iodine, strengthening public awarness on necessary increase of milk consumption especially in pregnancy and in children and continouse monitoring system of biologic effects and technologic quality of the model of iodine prophylaxis.
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PMID:[Iodine deficiency in pregnancy--a continuing public health problem]. 1633 75

Both epidemiological and experimental studies have shown that impaired growth in utero due to maternal malnutrition, resulting in low birth weight, is associated with a high incidence of glucose intolerance, insulin resistance, and type 2 diabetes in adult life. Maternal malnutrition is a worldwide problem and unavoidable; therefore, prevention of type 2 diabetes in low birth weight infants who reach adulthood is difficult to achieve. Administration of human umbilical cord blood (HUCB) mononuclear cells into type 1 and type 2 diabetic mice has been shown to improve both their blood glucose levels and survival. It has also been shown that the progenitor cells derived from HUCB improve not only glycemia but also other disease conditions, including systemic lupus erythematosis, amyotrophic lateral sclerosis, Alzheimer's disease, stroke, brain damage in animals and certain malignancies in humans. Transfusion of unrelated HUCB, although abundantly available, is underutilized as a therapeutic agent. Therefore, we propose the hypothesis that transfusion of HUCB to low birth weight infants be considered a therapeutic modality to prevent the development of type 2 diabetes in their adulthood.
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PMID:Administration of human umbilical cord blood to low birth weight infants may prevent the subsequent development of type 2 diabetes. 1648 Nov 20

Over the years, several clinical syndromes have been described in diabetes mellitus. Although world opinion has settled somewhat on the main two types, the debate continues as to how the 'formes frustes' syndromes fit in and what if any implications there are for the accepted aetiology of the disease. Type 1, insulin dependent diabetes mellitus, results from pancreatic inadequacy as a result of a variety of insults such as autoimmune attack, toxic damage, etc. Insulin administration is at the core of the therapeutic approach. Type 2, non insulin dependent diabetes mellitus, results from reduced responsiveness of the target tissues to insulin and as such, an insulin resistance syndrome is described. Lifestyle adjustment and oral hypoglycaemic agents are the mainstay of therapy. Over the years, however, insulin insufficiency will develop in most cases and insulin therapy required in order to achieve normoglycaemia. The aetiology of these main two types has been maintained to be distinct from each other and as such types 1 and 2 are described as two separate developmental conditions. Furthermore, the variant patterns, such as malnutrition related, drug induced, intermittent or phasic insulin requiring, gestational, temporary, stress related, etc., all present a challenge as to how they fit in aetiologically. The Unitarian Hypothesis, by presenting this overall cascade of biochemical and physiological interactions, brings a logic which embraces the points of entry of a variety of insults, all of which can lead to the clinical picture of hyperglycaemia and its attendant adverse outcomes. The hypothesis buttresses the belief that nature - the genetic predisposition which directs potential antibody development; and nurture - the environmental influences such as nutritional status (over- or under-), infective and toxic attack, can aggravate or initiate aspects of the cascade of reactions leading to hyperglycaemia. The causative agents functioning internally within the cascade are imputed to be free radicals, oxidizing molecular species and antibodies and the corollary to this overview concept would be that a situation that minimizes the genesis and accumulation of these three agents would minimize the development of diabetes mellitus. Currently the debate is rife about the use of free radical scavengers and antioxidants in the treatment and prevention of diabetes mellitus. The verdict is still out on this approach. Our research on rootcrops such as yams and cassava, staple foods in tropical countries, indicates the presence of cyanoglycosides such as linamarin, which on digestion yields cyanide radicals. These radicals are pancreatotoxic especially in the undernourished state. Dog models however, have shown that free radical scavengers such as riboflavin, Vitamin B(2), is protective against this toxic damage. Further, scientific investigations have clearly demonstrated the role of antibody attack and have been able to ward off the appearance of type 1 diabetes mellitus in susceptible individuals, by the early use of immunosuppressive therapy such as cyclosporin. Thus the Unitarian Hypothesis demonstrates how all types of clinical syndromes being described in diabetes mellitus are not necessarily variants of a specific illness but rather manifestations of a central process of membrane damage-->antibody response-->insulin inadequacy (quantitatively or qualitatively); and the future intervention in containing this disease may well lie in focusing on preservation of the integrity of the body's cell membranes.
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PMID:The Unitarian Hypothesis for the aetiology of diabetes mellitus. 1680 31

Epidemiological studies in humans suggest that maternal undernutrition, obesity and diabetes during gestation and lactation can all produce obesity in offspring. Animal models have allowed us to investigate the independent consequences of altering the pre- versus post-natal environments on a variety of metabolic, physiological and neuroendocrine functions as they effect the development in the offspring of obesity, diabetes, hypertension and hyperlipidemia (the 'metabolic syndrome'). During gestation, maternal malnutrition, obesity, type 1 and type 2 diabetes and psychological, immunological and pharmacological stressors can all promote offspring obesity. Normal post-natal nutrition can reduce the adverse impact of some of these pre-natal factors but maternal high-fat diets, diabetes and increased neonatal access to food all enhance the development of obesity and the metabolic syndrome in offspring. The outcome of these perturbations of the perinatal environmental is also highly dependent upon the genetic background of the individual. Those with an obesity-prone genotype are more likely to be affected by factors such as maternal obesity and high-fat diets than are obesity-resistant individuals. Many perinatal manipulations appear to promote offspring obesity by permanently altering the development of central neural pathways, which regulate food intake, energy expenditure and storage. Given their strong neurotrophic properties, either excess or an absence of insulin and leptin during the perinatal period are likely to be effectors of these developmental changes. Because obesity is associated with an increased morbidity and mortality and because of its resistance to treatment, prevention is likely to be the best strategy for stemming the tide of the obesity epidemic. Such prevention should begin in the perinatal period with the identification and avoidance of factors which produce permanent, adverse alterations in neural pathways which control energy homeostasis.
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PMID:Metabolic imprinting: critical impact of the perinatal environment on the regulation of energy homeostasis. 1681 95

Maternal malnutrition is known to impair fetal growth and predispose to the development of hypertension and type 2 diabetes. Recently, studies have demonstrated that intrauterine malnutrition is followed later in male offspring by oxidative stress characterized by increased superoxide generation due to activation of NADPH oxidase and reduced antioxidant defenses. However, few studies have investigated the mechanisms involved in endothelial dysfunction in female offspring. We evaluated the effects of the exogenous application of superoxide scavengers on the endothelium-dependent vasorelaxation in the mesenteric microvessels of female offspring. In addition, we examined indicative parameters of oxidative stress by measuring superoxide anion concentration and the activity of superoxide dismutase (SOD) as a marker of antioxidant defenses. Pregnant female Wistar rats were fed either a normal diet or 50% of this, throughout gestation. Intrauterine malnutrition induced hypertension and increased superoxide production without affecting SOD activity. Topical application of MnTMPyP (SOD mimetic) and apocynin (NADPH oxidase inhibitor) significantly improved the altered arteriolar responses to acetylcholine and bradykinin. In addition, incubation with apocynin reduced superoxide generation in these female offspring. The data suggest that after exposure to intrauterine malnutrition, female offspring present an increased superoxide production that is, at least in part, responsible for an endothelial dysfunction observed in these animals. These effects may be mediated via modulation of enzyme systems that generate superoxide.
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PMID:Long-term effects of intrauterine malnutrition on vascular function in female offspring: implications of oxidative stress. 1715 80

Awareness of a serious Indigenous health problem in Australia did not emerge until the 1960s and 1970s. Much attention was focused at the time on poor pregnancy outcomes, high infant and young child mortality rates, and childhood malnutrition and impaired growth, often associated with high infectious disease burdens. Although that situation has improved somewhat, Indigenous infant and child health is still poor compared with that of other Australian children. Over recent decades, there has been a rapid rise among Indigenous people of nutrition-related "lifestyle" disorders such as obesity, cardiovascular disease, type 2 diabetes mellitus and chronic renal disease and their complications. This epidemic of disabling and often fatal chronic diseases in Indigenous Australians is also occurring in disadvantaged groups in many other countries. Control of this potentially disastrous epidemic must become a much higher priority in Indigenous health programs. Governments must commit to this task in cooperation and collaboration with Indigenous organisations and communities.
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PMID:Nutrition-related disorders in Indigenous Australians: how things have changed. 1722 25

Obesity is recognized as a serious problem in the industrialized and developed countries of the world. However, little attention is paid to the fact that obesity is becoming an increasing problem in developing countries too, with some countries showing increasing rates of obesity in the midst of the persisting occurrence of childhood malnutrition and stunting. As developing countries embrace the dominant western economic ways of development, industrialization and urbanization they contribute to improvements in living standards, with consequent dramatic changes in diets and lifestyles leading to weight gain and obesity which in turn poses a growing threat to the health. Overweight and obesity is associated with an increased likelihood of non-insulin dependent diabetes mellitus, hypertension, hyper-lipidaemia, and cardiovascular disease. It is also associated with increased rates of breast, colo-rectal and uterine cancer. Obesity is thus an important factor in the increasing morbidity and mortality due to chronic, non-communicable diseases (NCDs) and thereby contributes to premature mortality in the population. Thus, while the problem of undernutrition persists in much of the developing world, overweight and obesity and its related co-morbidities are posing an increasingly important public health problem both in the developed and developing world.
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PMID:Introductory lecture the epidemiology and determinants of obesity in developed and developing countries. 1724 77

The next decade will face an increase in the number of patients affected by end-stage renal disease. In line with the growing incidence of type 2 diabetes, hypertension and old age in the general population, we can expect a dramatic increase of uremic patients needing a substitutive treatment of renal function. On the basis of the current trends, we expect an exponential growth of cardiovascular complications in both dialysis and transplant populations. Progress in the treatment of end-stage renal disease will aim at the prevention of cardiovascular complications, that remain the leading cause of morbidity and mortality in uremic patients. Preventive interventions for cardiovascular complications should focus on traditional risk factors, such as hypertension, dyslipidemia and obesity, diabetes mellitus, smoking, as well as on the non traditional risk factors inherent in the uremic state, such as anemia, hyperphosphoremia, hyperhomocysteinemia, inflammation and malnutrition. Recent and future innovations in peritoneal dialysis solutions include a larger use of icodextrin, a glucose polymer able to enhance ultrafiltration while inducing less glycation and caloric absorption, and perhaps improving blood pressure control. The gene therapy directed to the mesothelial cells should bring about improvements in nutrition, cardiovascular comorbidity, and dialysis adequacy. Patients submitted to increased hemodialysis time or to the implementation of a night or daily hemodialysis program have shown better blood pressure control, cardiovascular stability, tolerability and perhaps reduced mortality. Modifications of dialysis schedules clearly indicate another road to future improvements in renal replacement therapy. In the field of kidney transplantation, much improvement has already been achieved regarding the prevention of acute rejection, and the new therapeutic strategies are aimed at reducing the incidence of the adverse reactions of immunosuppressive drugs, as well as of the chronic allograft nephropathy. Induction of transplantation tolerance remains the most attractive target, which now seems closer than before because many of the mechanisms involved in the tolerance induction have been better elucidated.
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PMID:[Perspectives on treatment of the renal failure]. 1725 35


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