Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 23-year-old man suffering from Crohn's disease developed a bilateral maculopathy simulating 'cherry-red spot' with vision impairment and normal electroretinogram during total parenteral hyperalimentation, when copper and zinc serum levels were considerably decreased. The maculopathy rapidly subsided after cessation of the parenteral hyperalimentation and the addition of cooper and zinc. The cause of this maculopathy may be ocular involvement as part of the systemic disease owing to storage of the supplementary free amines and intravenous lipids, and the deficiency of zinc and copper.
 ...
PMID:Bilateral maculopathy simulating 'cherry-red spot' in a patient with Crohn's disease. 678 47

Two patients developed severe zinc deficiency with acrodermatitis during parenteral hyperalimentation. The response of circulating T-lymphocytes to phytohemagglutinin was assessed both during the episode of clinical zinc deficiency and after intravenous zinc supplementation as the sole means of nutritional intervention. Maximum T-cell response to phytohemagglutinin, expressed as percent of simultaneous normal control response, was 2.1% and 27.9% in Patients 1 and 2 respectively. After 20 days of intravenous zinc supplementation (12 mg/d), repeat studies showed the T-cell response of Patient 1 to be 221% of the control, and that of Patient 2 to be 139% of control. In addition, Patient 1 was anergic during the period of zinc deficiency and normally reactive after zinc supplementation. These findings agree with extensive animal studies showing the detrimental effect of zinc deficiency on cellular immunity.
 ...
PMID:Severe zinc deficiency in humans: association with a reversible T-lymphocyte dysfunction. 678 37

Rats fed a varied and palatable "cafeteria" diet exhibited hyperphagia, increases in resting metabolic rate (VO2) and the thermogenic response to noradrenaline as well as hypertrophy of brown adipose tissue (BAT). In streptozotocin-diabetic rats, cafeteria feeding failed to produce increases in VO2 or the response to noradrenaline, although BAT mass was greater than in their respective stockfed controls. Replacement doses of insulin (protamine-zinc-insulin, PZI) at two levels (2 and 4 units/rat every alternate day) failed to restore the thermogenic response of diabetic rats to the cafeteria diet. Acute replacement (8 units PZI) 12hr before the measurements resulted in resting and noradrenaline-stimulated values for VO2 that were similar to those of non-diabetic cafeteria rats. These findings suggest an insulin requirement for diet-induced thermogenesis and the failure of diabetic rats to maintain body temperature when exposed to cold (5 degrees C) suggests a further insulin requirement for cold-induced thermogenesis. In non-diabetic cafeteria rats, plasma insulin levels were significantly lower than those of stock fed controls in spite of a high carbohydrate intake and normal blood glucose.
 ...
PMID:A role for insulin in the diet-induced thermogenesis of cafeteria-fed rats. 701 42

Insulin stimulates the production of superoxide and hydrogen peroxide in various tissues. Hydrogen peroxide has been proposed to be an intracellular second messenger for insulin and a moderator of cellular proliferation and differentiation. We previously found that cell proliferation is increased in small intestinal mucosa of streptozotocin-diabetic rats. The current study was undertaken to determine if superoxide dismutase (SOD), the enzyme that converts superoxide to hydrogen peroxide, is altered in the mucosa of the alimentary tract and renal cortex of the diabetic rat, and if so, whether SOD responds to insulin treatment. Total SOD and cyanide-insensitive [manganese-containing SOD (Mn SOD)] SOD were measured by the nitroblue tetrazolium inhibition assay. We studied ad libitum fed animals, where diabetics are hyperphagic and pair-fed animals, where hyperphagia is not present. Since cyclic nucleotides appear to control cell proliferation in some tissues, we also measured cAMP and cGMP in mucosa of the small intestine. In ad libitum fed animals, total SOD was depressed in the mucosa of duodenum, jejunum, and ileum, but not in the cecum or colon of the streptozotocin-diabetic rats. The level of Mn-SOD was not affected by diabetes or insulin treatment, but the cyanide-sensitive [copper- and zinc containing SOD (Cu-Zn SOD] SOD was depressed in the small intestine and colon of diabetic rats. Insulin treatment restored total and Cu-Zn SOD activity in the small intestine to normal and increased Cu-Zn SOD activity in the colon to normal. Pair-fed animals showed the same changes in the SOD activity of jejunal mucosa that were found in ad libitum fed animals. In renal cortex, diabetes did not alter total SOD, but increased Mn SOD and decreased Cu-Zn SOD. Both responses were reversed by insulin treatment. Cyclic nucleotide concentrations were not affected by diabetes. We conclude that SOD enzymes re altered in diabetes, at least in proliferating tissues. Responses are tissue specific. The mucosa of the small intestine and colon show decreased Cu-Zn SOD, the SOD of the cecum is unaffected, and the kidney shows increased Mn SOD and decreased Cu-Zn SOD. The SOD responses of diabetics are reversed by insulin treatment.
 ...
PMID:Superoxide dismutase activity in the intestine of the streptozotocin-diabetic rat. 704 72

Dopamine (DA)-depleting brain lesions of various sizes were produced in rats either by intracerebroventricular injections of 6-hydroxydopamine (6-HDA) or by electrolytic lesions of the lateral hypothalamic (LH) area. Among 30 animals that became aphagic and adipsic for at least four days after large LH or 6-HDA-induced brain lesions, only three developed hyperphagia after electrolytic lesions of the ventromedial hypothalamus (VMH) or daily injections of long-acting protamine-zinc insulin (PZI). In 20 rats with smaller LH or 6-HDA-induced lesions, which had not shown marked initial behavioral dysfunctions, only three gained as much weight after VMH lesions as the control animals. Similarly, 6 of 10 rats with smaller LH lesions could not tolerate a 15-day series of PZI treatments, although 14 of 17 rats with smaller 6-HDA-induced lesions increased their food intake and gained weight during the PZI treatments as did control animals. These results indicate that hypothalamic hyperphagia can be blocked by DA-depleting brain lesions that neither produce an initial period of aphagia and adipsia nor involve hypothalamic tissue. They further indicate that even small LH lesions may prevent the development of hyperphagia elicited by PZI, whereas only very large 6-HDA-induced lesions consistently have this effect.
 ...
PMID:Effects of dopamine-depleting brain lesions on experimental hyperphagia in rats. 707 39

Plasma glucose concentration was measured at 3-h intervals in streptozotocin-induced diabetic rats placed on various insulin replacement regimens using three different kinds of insulin. High insulin dosages produced at least periodic hypoglycemia, even though there were no overt signs of insulin overdose. Low- and single-dose regimens produced periods of hyperglycemia. Both high and low doses of protamine zinc insulin normalized diabetes-induced reductions in 5-hydroxyindole-3-acetic acid [5-HIAA; the principal metabolite of 5-hydroxytryptamine (5-HT)] and 5-HT turnover (5-HIAA/5-HT), despite the failure of the low-dose regimen to normalize plasma glucose. Diabetic rats evidenced continued hyperphagia and hyperdipsia during insulin treatment, and insulin treatment also induced hyperphagia and excessive weight gain in nondiabetic rats. Insulin treatment only partially normalized diabetes-induced adrenal hypertrophy. Adrenal hypertrophy is an indication of a continued stresslike physiological state in diabetes even during insulin therapy. This state may be involved in the enhanced risk in diabetic humans for development of anxiety disorders and clinical depression.
 ...
PMID:Metabolic and neurochemical profiles in insulin-treated diabetic rats. 750 9

The proponents of fat-restricted diets for children argue that low-fat diets given in childhood will prevent the development of atherosclerosis in adulthood, low-fat diets given a childhood will condition children to prefer low-fat diets in adulthood, and low-fat diets for children are safe. There is no evidence that low-fat diets in childhood will prevent atherosclerosis in adulthood. In fact, studies of migrating populations indicate that immigrants to the United States from Third World countries who consumed low-fat diets in childhood take on the character of their new environments, including higher serum cholesterol levels and more coronary disease. The prevalence of fatty streaks in childhood bears little relationship to the prevalence of atheromatous plaques in adulthood. In fact, girls have more aortic fatty streaks and higher serum cholesterol values in childhood than boys, but fewer plaques in adulthood and less coronary disease. From the PDAY study, it has also been learned that hypercholesterolemia in childhood enhances fatty streak formation, but not that of plaques. It now seems established from autopsy studies that the progression of atherosclerosis from fatty streaks to plaque is arrested in childhood and does not begin to a significant extent until after puberty in males and after menopause in females. So the oft-repeated statement that atherosclerosis begins in childhood is semantically true but very misleading. The particularly harmful form of atherosclerosis (the plaque) does not become significant until much beyond puberty. The effects of low-fat, low-cholesterol diets on serum lipids and lipoproteins are of a lesser magnitude in children than in adults. The 0.78 mmol/L decrease in LDL cholesterol in the intervention group from controls (change 1.5%) in the DISC study was biologically insignificant and reflects the tighter control of lipoprotein and cholesterol synthesis in children compared with adults. It must be remembered that the human body synthesizes all of the cholesterol it needs from acetyl CoA. In general, the larger the amount of dietary cholesterol absorbed, the smaller the rate of biosynthesis of cholesterol. In some adults and most children this homeostatic control is nearly perfect, but in many adults the correction in biosynthesis of cholesterol with increased dietary input is imperfect and LDL cholesterol values increase. The second argument of the proponents of low-fat diets for children is that they are conditioned to continue low-fat diets in adulthood. From the studies of Birch and Fisher (51) this prediction seems unlikely. These investigators found that restricting access to palatable foods enhanced the interest of 3- to 5-year-old children in those foods and increased their desire to obtain and consume those foods. They concluded that "stringent parental controls can potentiate preference for high-fat energy-dense foods, limit children's acceptance of a variety of foods and disrupt children's regulation of energy intake." Brosin (52) has also observed that food restriction in childhood may lead to gluttony in adulthood. Finally, the claim that low-fat diets are safe in childhood is based on observations over too short a time to establish safety. It is true that growth and development of children studied in the DISC study was not changed from the expected increments, but that is not proof of long-term safety. In addition, the lower content of essential nutrients in low-fat, low-cholesterol diets (calcium, zinc, magnesium, phosphorus, vitamin E, vitamin B-12, thiamin, niacin, and riboflavin) must be considered along-term risk (53,54). Furthermore, the published studies of the safety of low-fat diets have been conducted under intensive surveillance in medical centers, conditions very different from those in the homes of free-living families.
 ...
PMID:Is it wise to restrict fat in the diets of children? 1064 98

Although the Mexican population has traditionally been malnourished, the prevalence of obesity in children and adults has increased by almost 50 % in the last 10 years. Recent studies show substantial changes in the nutritional status of Mexicans, especially in the pediatric population. Among the factors associated with the development of obesity are overeating, sedentariness, and genetics. The apparent economic development in Mexico, as well as the influence of dietary patterns from other countries, have contributed to modifying lifestyle. Despite measures taken by the health system, iron- and zinc-deficiency anemia continue to be prevalent. The present review aims to describe the changes that have taken place in Mexico in the last few decades leading to a generation of short and obese children, as well as to determine the associated factors in order to promote healthier eating patterns among the Mexican population.
 ...
PMID:[Dietary changes in Mexico]. 1278 Nov 13

Youth, 9-18 years (n = 202), living in homeless shelters in Minneapolis, Minnesota, were assessed for height, weight, dietary intake, and perceptions of food insecurity. Perceptions of food security were measured by asking youth to respond to the statements (1) "There are times when we do not have enough food in the house," (2) "I go to bed hungry at night," (3) "I do not get enough to eat at home," and (4) "Have you ever had to miss a meal (or not been able to eat) because there was no food at home?" Additionally, questions evaluated coping mechanisms used by children to ward off hunger. Fifty-five percent of the children reported not enough food in the house and 25% reported going to bed hungry. Youth had inadequate intakes of vitamin D, calcium, and potassium and the majority consumed less than the estimated average requirements (EAR) for vitamins A, C, and E, phosphorus, folate, and zinc. Fruits, vegetables, and dairy were also consumed below recommended levels. Forty-five percent of boys and 50% of girls were at risk-for-overweight or were overweight. Overeating, eating anything, eating disliked foods, and eating at the homes of family and friends were identified as strategies to cope with food insecurity. Overeating when food is available may explain why we see a hunger-obesity paradigm to the magnitude that we do among the poorest Americans. These strategies protect children from the immediate negative associations of poverty and hunger, but they may contribute to long-term weight problems currently found in the US.
 ...
PMID:Dietary intake, overweight status, and perceptions of food insecurity among homeless Minnesotan youth. 1849 7

Branched-chain ketoacid dehydrogenase deficiency results in complex and volatile metabolic derangements that threaten brain development. Treatment for classical maple syrup urine disease (MSUD) should address this underlying physiology while also protecting children from nutrient deficiencies. Based on a 20-year experience managing 79 patients, we designed a study formula to (1) optimize transport of seven amino acids (Tyr, Trp, His, Met, Thr, Gln, Phe) that compete with branched-chain amino acids (BCAAs) for entry into the brain via a common transporter (LAT1), (2) compensate for episodic depletions of glutamine, glutamate, and alanine caused by reverse transamination, and (3) correct deficiencies of omega-3 essential fatty acids, zinc, and selenium widespread among MSUD patients. The formula was enriched with LAT1 amino acid substrates, glutamine, alanine, zinc, selenium, and alpha-linolenic acid (18:3n-3). Fifteen Old Order Mennonite children were started on study formula between birth and 34 months of age and seen at least monthly in the office. Amino acid levels were checked once weekly and more often during illnesses. All children grew and developed normally over a period of 14-33 months. Energy demand, leucine tolerance, and protein accretion were tightly linked during periods of normal growth. Rapid shifts to net protein degradation occurred during illnesses. At baseline, most LAT1 substrates varied inversely with plasma leucine, and their calculated rates of brain uptake were 20-68% below normal. Treatment with study formula increased plasma concentrations of LAT1 substrates and normalized their calculated uptakes into the nervous system. Red cell membrane omega-3 polyunsaturated fatty acids and serum zinc and selenium levels increased on study formula. However, selenium and docosahexaenoic acid (22:6n-3) levels remained below normal. During the study period, hospitalizations decreased from 0.35 to 0.14 per patient per year. There were 28 hospitalizations managed with MSUD hyperalimentation solution; 86% were precipitated by common infections, especially vomiting and gastroenteritis. The large majority of catabolic illnesses were managed successfully at home using 'sick-day' formula and frequent amino acid monitoring. We conclude that the study formula is safe and effective for the treatment of classical MSUD. In principle, dietary enrichment protects the brain against deficiency of amino acids used for protein accretion, neurotransmitter synthesis, and methyl group transfer. Although the pathophysiology of MSUD can be addressed through rational formula design, this does not replace the need for vigilant clinical monitoring, frequent measurement of the complete amino acid profile, and ongoing dietary adjustments that match nutritional intake to the metabolic demands of growth and illness.
 ...
PMID:Classical maple syrup urine disease and brain development: principles of management and formula design. 2006 Nov 71


<< Previous 1 2 3 4 Next >>