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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A survey of mothers attending infant welfare clinics showed that 26% changed their infant's milk in the first two weeks after birth and that multiple changes were common. Twenty-two per cent. were preparing a milk formula more concentrated than the recommended strength by using either heaped or packed scoops instead of level scoops of powder or by giving extra scoops. The commonest age for starting solid feeding was between 3 and 4 weeks and the practice of adding rusk or cereal to the bottle was common. There are obvious dangers of hypernatraemia from taking concentrated milk feeds and problems of obesity which may follow the early introduction of cereals.
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PMID:Infant-feeding practices. 474 Apr 63

Many authors have pointed that precocious weaning expose infants to serious risks as hypernutrition, obesity, adverse reactions to foods, hypernatremia, dental caries, emotional problems as anorexia or bulimia, so that actually weaning is delayed after 6th month of age. Going on with the "adapted" formula is a relative nonsense because "adapted" milks have low protein and calcium contents so that they are not adequate to cover estimated and advisable intakes of 4-6 month baby unless feeding unusual higher volumes. On the other side "fresh milk" can not be considered a nutritional "chance", owing its low values of EFA, iron, vitamins, getting worse when fresh milk is diluted. So, recently was born a new milk formula "the follow up milk", on covering nutritional requirement for infants after 4 months of age. Someone is still critical about a follow up milk, also if ESPGAN in 1981 has confirmed its value in the infant feeding. Our work dealed on physical and biochemical nutritional assessment of 100 infants fed a new "liquid follow up formula" (Transilat). Nutritional assessment was performed with the following parameters: daily changes in weight according Fomon standards, plasmatic iron, cholesterol, transferrin, calcium, total proteins, hemoglobin concentration; all data are related to literature values for age. Results show that infants fed (Transilat) are growing well; nutritional data from biochemical point of view discovered any form of minimal or sporadic malnutrition. The follow up milk is a good nutritional "chance" after 4th month of age, instead of fresh cow milk; some infant with clinical problem needing a delayed introduction of cow milk can benefit of follow up milk also in older ages.
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PMID:["Follow-up milk": general principles and evaluation of the nutritional status of 100 subjects fed a liquid transitional formula]. 664 69

The clinical and laboratory data of a 5-year-old boy with the syndrome of essential hypernatremia are presented. In a four-year follow-up, no demonstrable hypothalamic structural lesion has been identified. Review of the literature has uncovered four similar cases, suggesting a distinct syndrome of altered hypothalamic function. The syndrome is characterized by: adipsia-hypodipsia (5/5 patients), recurrent hypernatremia (5/5), obesity (4/5), inability to excrete a water load (5/5), lack of growth hormone release in response to provocative stimuli (4/4), blunted thyrotropin releasing hormone responses (3/4), hypothyroidism (2/4), and hyperlipemia associated with hypernatremic crisis (1/1). In one of the patients the syndrome has been attributed to a disturbance of the opioid-peptide system.
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PMID:Hypothalamic adipsia without demonstrable structural lesion. 680 52

We report the case of a 9-year-old girl with multiple problems due to hypothalamic dysfunction of obscure origin: apnoeic spells, behavioural problems, developmental delay, hypodipsia with bouts of hypernatraemia, episodes of spontaneous hypothermia, obesity, petit-mal seizures, non-progressive precocious puberty, absence of respiratory response to CO2 and probably insensitivity of hyposensitivity to pain. She also had hyperprolactinaemia and decreased human growth hormone secretion. Hypothyroidism of central origin and hyposecretion of cortisol were also present. Multiple brain CT-scans failed to reveal any tumour or other anatomical abnormality. Her clinical course was improved initially by treatment with clomipramine, but she died suddenly, and the autopsy failed to disclose any anatomical lesion. We compare this case with three similar previously reported cases.
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PMID:Hypothalamic dysfunction in a child: a distinct syndrome? Report of a case and review of the literature. 768 46

Idiopathic hypothalamic dysfunction is a rare but well-defined entity in childhood characterized by adipsia-hypernatremia, obesity, poor thermoregulation, and disturbance of pituitary function. Two cases of idiopathic hypothalamic dysfunction are described. There are 10 previously reported cases in the literature, and the clinical features are compared. The present cases are unique in that the patients also had bilaterally dilated unresponsive pupils. In the first case, there was no demonstrable pathology at autopsy; in the second case, lymphocytic infiltration of the hypothalamus and midbrain associated with neuronal loss was present at autopsy. Possible etiologies are discussed.
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PMID:Idiopathic hypothalamic dysfunction with dilated unresponsive pupils: report of two cases. 793 Apr 14

Association between insulin resistance and hypertension: Insulin resistance and reactive hyperinsulinemia occur not only with obesity, impaired glucose tolerance or non-insulin-dependent (type 2) diabetes mellitus, but also in many non-obese, non-diabetic patients with essential hypertension and their currently normotensive, lean young offspring and in some other conditions known to promote hypertension. Insulin resistance impairs glucose tolerance, while insulin resistance and/or hyperinsulinemia promote dyslipidemia, body fat deposition and probably atherogenesis. Therefore, the common coexistence of a genetic predisposition for hypertension with insulin resistance helps to explain the frequent, although temporally often dissociated, occurrence of hypertension as well as dyslipidemia, obesity and type 2 diabetes in a given subject. Pathogenetic mechanisms: In the pathogenesis of hypertension, inappropriate vasoconstriction (due to dysbalance of vasoactive substances and/or raised cytosolic Ca2+) and/or a structural vasculopathy is a very important ultimate causative event. In the presumed mosaic of participating pressor mechanisms, distinct Na+ retention is almost obligatory with diabetes mellitus, while essential and particularly obesity-associated hypertension probably involves a tendency for sympathetic activation. Development of insulin resistance: Insulin resistance may develop as a consequence of an intracellular excess of Ca2+ or decrease in Mg2+, an impaired insulin-mediated rise in skeletal muscle blood flow, increased sympathetic activity or being overweight. Acute hyperinsulinemia on the one hand causes arterial vasodilation and on the other hand enhances renal sodium reabsorption and sympathetic activity. Chronically, hyperinsulinemia may promote cardiovascular muscle cell proliferation and atherogenesis, and it has been proposed that insulin resistance in certain transmembranous cation exchange systems may elevate cytosolic Ca2+. Nevertheless, whether insulin resistance and/or hyperinsulinemia itself contribute to the pathogenesis of hypertension is still unclear.
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PMID:Insulin resistance, hyperinsulinemia and hypertension. 815 79

This study examined the control of renal hemodynamics and tubular function, as well as systemic hemodynamics, during obesity-induced hypertension in chronically instrumented conscious dogs. Mean arterial pressure, cardiac output, and heart rate were monitored 24 hours a day using computerized methods, water and electrolyte balances were measured daily, and renal hemodynamics were measured each week during the control period and 5 weeks of a high-fat diet. After 7 to 10 days of control measurements, 0.5 to 0.9 kg of cooked beef fat was added to the regular diet, and sodium intake was maintained constant at 76 mmol/d throughout the study. After 5 weeks of the high-fat diet, body weight increased from 24.0 +/- 1.0 to 35.9 +/- 4.9 kg, mean arterial pressure increased from 83 +/- 5 to 100 +/- 4 mm Hg, cardiac output increased from 2.86 +/- 0.27 to 4.45 +/- 0.55 L/min, and heart rate rose from 68 +/- 5 to 107 +/- 9 beats per minute. Associated with the hypertension was an increase in cumulative sodium balance to 507 +/- 107 mmol after 35 days and a rise in sodium iothalamate space, an index of extracellular fluid volume, to 131 +/- 4% of control. Sodium retention was due to increased tubular reabsorption, because glomerular filtration rate and effective renal plasma flow increased throughout the 5 weeks of the high-fat diet, averaging 135 +/- 4% and 149 +/- 19% of control, respectively, during the fifth week of the high-fat diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Obesity-induced hypertension. Renal function and systemic hemodynamics. 834 21

GENETIC PREDISPOSITION: Insulin resistance and reactive hyperinsulinemia occur not only with obesity, impaired glucose tolerance or non-insulin-dependent (type 2) diabetes mellitus, but also in many non-obese, non-diabetic patients with essential hypertension and their currently normotensive, lean, young offspring, as well as in some other conditions known to promote hypertension. Insulin resistance impairs glucose tolerance, while insulin resistance and/or hyperinsulinemia promote dyslipidemia, body fat deposition and probably atherogenesis. Therefore, the common coexistence of a genetic predisposition for hypertension with insulin resistance helps to explain the frequent, although temporally often dissociated, occurrence of hypertension together with dyslipidemia, obesity and type 2 diabetes in a given patient. INSULIN RESISTANCE AND HYPERINSULINEMIA AS SLOW PRESSOR MECHANISMS: In the pathogenesis of hypertension, inappropriate vasoconstriction (due to an imbalance of vasoactive substances and/or raised cytosolic calcium) and/or structural vasculopathy is particularly important. Among the mosaic of assumed pressor mechanisms, distinct Na+ retention is almost invariably involved in diabetes mellitus, while sympathetic activation tends to occur in essential hypertension, particularly in association with obesity. Insulin resistance may develop as a consequence of an intracellular excess of Ca2+ or a decrease in Mg2+, an impaired insulin-mediated rise in skeletal muscle blood flow, increased sympathetic activity or excess body weight. Acute hyperinsulinemia causes arterial vasodilation on one hand and increases sympathetic activity and renal Na+ reabsorption on the other. Chronically, hyperinsulinemia may promote cardiovascular muscle cell proliferation and atherogenesis, while insulin resistance may be associated with certain transmembraneous cation transporters, leading to an increase in cytosolic Ca2+. Hyperinsulinemia and/or insulin resistance may also be associated with an increased blood pressure sensitivity to high salt intake. In the mosaic of many different blood pressure-raising mechanisms, insulin resistance and/or hyperinsulinemia is likely to represent an amplifying slow or very slow pressor factor.
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PMID:Insulin resistance and hyperinsulinemia in hypertension. 857 90

Obesity, currently affecting >20% of the adult population in most Western countries, is a major risk factor for the development of hypertension. Hypertension in obese patients is, in the majority of instances, further complicated by the concomitant presence of dyslipidemia and insulin resistance. The latter is reflected by derangement of glucose homeostasis, ranging from hyperinsulinemia to frank type 2 diabetes. Hypertension in obese patients is also associated with an increased risk for left ventricular hypertrophy, endothelial dysfunction, renal hyperfiltration, microalbuminuria, and elevated markers of inflammation. Sodium retention, volume expansion, and increased cardiac output are common findings in obese individuals. These changes are largely attributable to increased activity of the sympathetic nervous system and insufficient suppression of the renin-angiotensin system. Recent data show increased expression of angiotensin II-forming enzymes in adipose tissue, and increased activity of the renin-angiotensin system has recently been implicated in the development of insulin resistance and type 2 diabetes. Accordingly, antihypertensive agents that block the renin-angiotensin system might be a beneficial strategy for treatment of obesity-related hypertension. Both angiotensin-converting enzyme inhibitors and angiotensin type-1 receptor blockers have been associated with favorable metabolic properties and end-organ protection in addition to their antihypertensive effects. Data from ongoing large trials will provide an indication of the protective and preventive effects of these treatment strategies while offering insights into the mechanisms linking obesity, hypertension, and other facets of the metabolic syndrome.
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PMID:Is there a rationale for angiotensin blockade in the management of obesity hypertension? 1517 27

The process whereby a stimulus or stress at a critical or sensitive period of development has long-term effects is termed "programming." Studies in humans and animals convincingly demonstrate that environmental perturbations in utero may permanently change organ structure and metabolism and/or alter homeostatic regulatory mechanisms among the offspring. These programmed changes may be the origins of adult diseases, including cardiovascular disease, obesity, and diabetes. Throughout evolution and development, humans and animals have been exposed to two common environmental stresses, drought and famine. Notably, drought-induced water deprivation is associated with dehydration anorexia and thus a concomitant potential nutrient stress. Our laboratory has performed studies among pregnant rat and sheep in which we simulate drought conditions via maternal dehydration and famine conditions via nutrient restriction. Maternal dehydration results in low-birth-weight offspring, which demonstrate gender-specific plasma hypernatremia and hypertonicity and arterial hypertension. Gestational nutrient restriction also resulted in low-birth-weight offspring. If permitted rapid catch-up growth by nutrient availability, these offspring demonstrate evidence of increased body weight and body fat, and leptin resistance as adults. Conversely, if the catch-up growth is delayed by nutrition restriction, the offspring exhibit normal body weight, body fat, and plasma leptin levels as adults. These studies indicate that osmoregulatory and cardiovascular homeostasis and phenotypic predisposition to obesity may be programmed in utero. Importantly, these results suggest that programming effects may be either potentiated or prevented by interventions during the neonatal period.
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PMID:Gestational programming: population survival effects of drought and famine during pregnancy. 1559 Sep 94


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