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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diet therapy is an important factor in overall care of most GI patients. Historically, diets have been used unscientifically in many of these patients without positive results. Nutritional care and diet therapy are critical for two reasons. First, malnutrition is an expected sequelae to most, if not all, GI diseases or disorders. Failure to eat, digest, or assimilate nutrients can provoke malnutrition in just a few weeks, although careful assessment of anthropometric, clinical, biochemical, and nutritional history by a trained professional can protect against this. Diet therapy through the elimination of offending foods such as wheat gluten or lactose, or inclusion of specialized products such as medium chain triglycerides or elemental formulas, can sustain nutritional status. Dietary components such as insoluble fiber appear to have physiologic effects, while soluble fibers may have metabolic effects important to diabetes and cardiovascular disease. There is a high potential for malnutrition in Crohn's disease during active and remittent phases. Elemental enteral formulas or TPN are used during the active phase to ensure optimal nutritional status and bowel rest. Hyperalimentation using the GI tract during remittent stage maintains this. Avoiding offending foods by Crohn's patients is an acceptable practice as long as entire categories of foods are not deleted. Avoiding all foods containing gluten from wheat, rye, barley, and oats, however, is a crucial prerequisite to recovery from celiac disease. Gluten is commonly used as a stabilizer, emulsifier, and extender in the food industry and is not always shown on food labels. Careful consultation with a registered dietitian can identify hidden sources of gluten in the diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dietary therapy in gastrointestinal disease. 264 90

The incidence of coronary artery disease only weakly correlates with the percent of excess body weight; however, obesity in humans is not a homogeneous condition. Classification of obesity based on anatomic distribution of body fat allows for identification of a group of patients at increased risk for cardiovascular disease. Abdominal (upper body) obesity, measured as the waist/hip ratio, is a strong independent risk factor of cardiovascular disease and should be used to assess a subgroup in need of medical weight loss treatment. A focus on dietary fat intake and the magnitude of overeating "caloric intake" are central to the pathogenesis of cardiovascular disease observed in the obese person. Identification of the process of overeating (magnitude of recent weight gain, episodes of weight cycling) is important in the design of successful medical nutrition treatment programs. A nutrition/medical history that includes age of obesity onset and duration of obesity provides additional criteria for assessment of risk of disease. Childhood-onset obesity and prolonged obesity (greater than 15 years) has been associated with increased cardiovascular disease risk. Recently, grades of obesity based on body mass index have provided a valuable marker for treatment. Each reduction in obesity grade (equal to delta 5 body mass index or delta 11.6 kg) is associated with a decrease in risk of medical illness. The new focus of obesity treatment should be to decrease body weight in 10% to 15% increments (equal to 1 grade) with emphasis on reducing the risk of medical illness and treatment intensity (e.g., number of existing medical visits, hospitalization).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Medical evaluation and treatment of the obese patient with cardiovascular disease. 331 51

The treatment for pulmonary edema with the adult respiratory distress syndrome is aimed at the early supportive management of hypovolemic shock. The addition of massive corticosteroid dosage, Methylprednisolone Succinate, of 30 mg/kg body wt/dose ever six hours for a 24-48 hour period has been shown in our investigation to be efficacious, particularly in the traumatic and septic shock groups of patients but not in patients with multiple system diseases. Ventilator care utilizing constant positive pressure breathing or constant positive airway pressure in the patient who has spontaneous respirations is of prime importance. The recent utilization of hyperalimentation has also been very effective as an adjunctive therapy and should be used in the management of this problem in the future in conjunction with the steroids. Hemodynamic monitoring employing the specific parameters as delineated in our discussion are all major steps that should be pursued on a routine basis in the vast majority of these patients. The most important factor in the prognosis of this condition is the severity and number of injuries that have occurred at the time of the initial trauma. Other factors affecting the outcome are age, prolonged shock, associated degenerative cardiovascular disease, metabolic imbalance, severe multiple system involvement, and sepsis. We now feel that the utilization of massive corticosteroid therapy is indicated with the first earliest clinical signs of this condition in order to attempt to prevent complications and probably improve survival rate.
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PMID:Acute pulmonary edema with respiratory failure--newer concepts in therapy. 675 Nov 64

Obesity is associated with an increased incidence of infection, diabetes, and cardiovascular disease, which together account for most obesity-related morbidity and mortality. Decreased expression of leptin or of functional leptin receptors results in hyperphagia, decreased energy expenditure, and obesity. It is unclear, however, whether defective leptin-dependent signal transduction directly promotes any of the conditions that frequently complicate obesity. Abnormalities in tumor necrosis factor alpha expression have been noted in each of the above comorbid conditions, so leptin deficiency could promote these complications if leptin had immunoregulatory activity. Studies of rodents with genetic abnormalities in leptin or leptin receptors revealed obesity-related deficits in macrophage phagocytosis and the expression of proinflammatory cytokines both in vivo and in vitro. Exogenous leptin up-regulated both phagocytosis and the production of proinflammatory cytokines. These results identify an important and novel function for leptin: up-regulation of inflammatory immune responses, which may provide a common pathogenetic mechanism that contributes to several of the major complications of obesity.
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PMID:Leptin regulates proinflammatory immune responses. 943 11

Postprandial hyperlipidemia (PH) is recognized as a significant risk factor for cardiovascular disease. The present study, involving rats with streptozotocin (STZ)-induced diabetes, was performed to establish a PH model and to examine the relation between small intestinal acyl-coenzyme A:cholesterol acyltransferase (ACAT) activity and serum lipid levels in the postprandial state. The small intestinal ACAT activities in normal rats during the experimental period were 4 to 5 pmol/mg protein per minute. In contrast, in the diabetic rats, the ACAT activities were 2 to 3 times higher than activities seen in normal rats from 7 to 21 days after the STZ injection in the absence of a high fat diet and hyperplasia in the gut. In an oral fat-loading test that used diabetic rats that had been injected with STZ (60 mg/kg) intravenously 14 days previously, the postloading changes in the serum concentrations of total cholesterol (TC) and triglyceride (TG) were significantly greater in the diabetic rats than in normal rats. Single oral administration of (1s,2s)-2-[3-(2,2-dimethylpropyl)-3-nonylureido]cyclohexane- 1-yl 3-[(4R)-N-(2,2,5,5-tetramethyl-1, 3-dioxane-4-carbonyl)amino]propionate (F-1394, 3 to 30 mg/kg), a potent ACAT inhibitor, suppressed the post-fat-loading elevation of serum TC levels in the diabetic rats in a dose-dependent manner without affecting serum glucose levels. Furthermore, the small intestinal ACAT activity, serum TG levels, and lymphatic absorption of TC and TG in the rats that were administered F-1394 (30 mg/kg) were reduced by approximately 90%, 70%, 30%, and 15%, respectively. This is the first evidence that elevated ACAT activity in the gut, unlike hyperplasia and hyperphagia, induces PH in rats. Our results strongly suggest that F-1394 may be a potential treatment for PH in humans.
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PMID:Postprandial hyperlipidemia in streptozotocin-induced diabetic rats is due to abnormal increase in intestinal acyl coenzyme A:cholesterol acyltransferase activity. 1063 14

It is remarkable that neurons are able to survive and function for a century or more in many persons that age successfully. A better understanding of the molecular signaling mechanisms that permit such cell survival and synaptic plasticity may therefore lead to the development of new preventative and therapeutic strategies for age-related neurodegenerative disorders. We all know that overeating and lack of exercise are risk factors for many different age-related diseases including cardiovascular disease, diabetes and cancers. Our recent studies have shown that dietary restriction (reduced calorie intake) can increase the resistance of neurons in the brain to dysfunction and death in experimental models of Alzheimer's disease, Parkinson's disease, Huntington's disease and stroke. The mechanism underlying the beneficial effects of dietary restriction involves stimulation of the expression of 'stress proteins' and neurotrophic factors. The neurotrophic factors induced by dietary restriction may protect neurons by inducing the production of proteins that suppress oxyradical production, stabilize cellular calcium homeostasis and inhibit apoptotic biochemical cascades. Interestingly, dietary restriction also increases numbers of newly-generated neural cells in the adult brain suggesting that this dietary manipulation can increase the brain's capacity for plasticity and self-repair. Work in other laboratories suggests that physical and intellectual activity can similarly increase neurotrophic factor production and neurogenesis. Collectively, the available data suggest the that dietary restriction, and physical and mental activity, may reduce both the incidence and severity of neurodegenerative disorders in humans. A better understanding of the cellular and molecular mechanisms underlying these effects of diet and behavior on the brain is also leading to novel therapeutic agents that mimick the beneficial effects of dietary restriction and exercise.
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PMID:Neuroprotective signaling and the aging brain: take away my food and let me run. 1111 86

The discovery of a link between in utero experience and later metabolic and cardiovascular disease is one of the most important advances in epidemiology research of recent years. There is increasing evidence that alterations in the fetal environment may have long-term consequences on cardiovascular, metabolic, and endocrine pathophysiology in adult life. This process has been termed programming, and we have shown that undernutrition of the mother during gestation leads to programming of hyperphagia, obesity, hypertension, hyperinsulinemia, and hyperleptinemia in the offspring. Using this model of maternal undernutrition throughout pregnancy combined with postnatal hypercaloric nutrition of the offspring, we examined the effects of IGF-I therapy. Virgin Wistar rats (age 75 +/- 5 d, n = 20 per group) were time mated and randomly assigned to receive food either ad libitum or 30% of ad libitum intake (UN) throughout pregnancy. At weaning, female offspring were assigned to one of two diets (control or hypercaloric [30% fat]). Systolic blood pressure was measured at day 175 and following infusion with 3 microg/g per day recombinant human IGF-1 (rh-IGF-I) by minipump for 14 d. Before treatment, UN offspring were hyperinsulinemic, hyperleptinemic, hyperphagic, obese, and hypertensive on both diets, compared with ad libitum offspring and this was exacerbated by hypercaloric nutrition. IGF-I treatment increased body weight in all treated animals. However, systolic blood pressure, food intake, retroperitoneal and gonadal fat pad weights, and plasma leptin and insulin concentrations were markedly reduced with IGF-I treatment. IGF-I treatment resulted in a 3- to 5-fold increase in 38--44 kDa and 28--30 kDa IGF binding proteins, although in UN animals, there was an impaired and differential up-regulation of these insulin-like growth factor binding proteins following IGF-I treatment. The 24-kDa IGF binding protein representing IGF binding protein-4 was down-regulated in all IGF-I-treated animals, but the decrease was more marked in UN animals. Our data suggest that IGF-I treatment alleviates hyperphagia, obesity, hyperinsulinemia, hyperleptinemia, and hypertension in rats programmed to develop the metabolic syndrome X.
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PMID:IGF-I treatment reduces hyperphagia, obesity, and hypertension in metabolic disorders induced by fetal programming. 1151 75

Diabetes mellitus, caused by the malfunction of insulin-dependent glucose and lipid metabolism, presents with the classical triad of symptoms: polydypsia, polyuria, and polyphagia which are often accompanied by chronic fatigue and loss of weight. Complications of diabetes mellitus include retinopathy, nephropathy, neuropathy, and cardiovascular disease. Periodontal diseases are infections affecting the periodontium and resulting in the loss of tooth support. The association between diabetes mellitus and periodontitis has long been discussed with conflicting conclusions. Both of these diseases have a relatively high incidence in the general population (diabetes 1% to 6% and periodontitis 14%) as well as a number of common pathways in their pathogenesis (both diseases are polygenic disorders with some degree of immunoregulatory dysfunction). On the one hand, numerous reports indicate a higher incidence of periodontitis in diabetics compared to healthy controls, while other reports fail to show such a relationship. Clarification of this dilemma is occurring as the diagnostic criteria for periodontitis and diabetes mellitus improve, controlled studies with increased sample sizes are carried out, and the studies take into account major confounding variables that impact on the pathogenesis of both diseases. Current studies tend to support a higher incidence and severity of periodontitis in patients with diabetes mellitus. The overview looks at the bidirectional relationship between periodontitis and diabetes. An analysis of the National Health and Nutrition Examination Survey (NHANES) III data set confirms the previously reported significantly higher prevalence of periodontitis in diabetics than in non-diabetics (17.3% versus 9%). The analysis of the data also shows that the prevalence of diabetes in patients with periodontitis is double that seen in the non-periodontitis patients (12.5% versus 6.3%) and that this difference is also statistically significant. The pathogenesis of the 2 diseases is reviewed with an emphasis on common genetic and immune mechanisms. On the basis of the overview, 2 hypotheses for testing the relationship between periodontitis and diabetes are discussed. The first proposes a direct causal or modifying relationship in which the hyperglycemia and hyperlipidemia of diabetes result in metabolic alterations that may then exacerbate bacteria-induced inflammatory periodontitis. The second hypothesis proposes that a fortuitous combination of genes (gene sets) could result in a host who, under the influence of a variety of environmental stressors, could develop either periodontitis or diabetes or both.
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PMID:The relationship between periodontal diseases and diabetes: an overview. 1188 77

Overfeeding and overeating in families are traditions that are often transferred from generation to generation. Irrespective of these family traditions, food availability might lead to overfeeding, in its turn leading to metabolic adaptations. Apart from selection, could these adaptations to the social environment have transgenerational effects? This study will attempt to answer the following question: Can overeating during a child's slow growth period (SGP), before their prepubertal peak in growth velocity influence descendants' risk of death from cardiovascular disease and diabetes? Data were collected by following three cohorts born in 1890, 1905 and 1920 in Overkalix parish in northern Sweden up until death or 1995. The parents' or grandparents' access to food during their SGP was determined by referring to historical data on harvests and food prices, records of local community meetings and general historical facts. If food was not readily available during the father's slow growth period, then cardiovascular disease mortality of the proband was low. Diabetes mortality increased if the paternal grandfather was exposed to a surfeit of food during his slow growth period. (Odds Ratio 4.1, 95% confidence interval 1.33-12.93, P=0.01). Selection bias seemed to be unlikely. A nutrition-linked mechanism through the male line seems to have influenced the risk for cardiovascular and diabetes mellitus mortality.
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PMID:Cardiovascular and diabetes mortality determined by nutrition during parents' and grandparents' slow growth period. 1682 95

Traditional cardiology has taken a mechanistic approach to heart disease. But the new discipline of behavioral cardiology takes a broader view, concluding that heart disease is not inevitable, but develops largely from unhealthy lifestyles, such as smoking, overeating and physical inactivity, and from psychosocial stress. Physical inactivity and excessive caloric intake are also responsible for the epidemic of obesity, which is associated with a dramatic increase in the prevalence of diabetes. This increase in the incidence of diabetes may, in turn, reverse the recent decline of cardiovascular deaths in the US. A variety of psychosocial stressors have been implicated in the development of cardiovascular disease. These include occupational stress, anxiety, social isolation, hostility, anger, and type A behavior. There is clearly some overlap between these stressors, all of which may affect the heart adversely. Both the lifestyle and psychosocial factors can be altered by behavioral treatment, in which the patient and the practitioner work together. Unfortunately, various barriers can impair the successful implementation of behavioral treatment. These barriers include poor compliance by the patient, lack of skill in providing effective interventions by the health care provider, and lack of incentives within the health care system, particularly reimbursement.
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PMID:Behavioral cardiology --has its time finally arrived? 1263 2


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