Gene/Protein Disease Symptom Drug Enzyme Compound
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 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review begins with James Olds' discovery that self-stimulation at various brain sites can be influenced by food intake or androgen treatment. It then describes our research designed to reveal the functional significance of self-stimulation. The evidence suggests that lateral hypothalamic self-stimulation is controlled by many of the same factors that control feeding. We believe this control is exerted by at least two neural mechanisms. One is the classical, medial hypothalamic satiety system. Another is an adrenergic system ascending from the midbrain to the lateral hypothalamus. Damage to either one can disinhibit self-stimulation and feeding, thus contributing to obesity. Some of our studies use rats with two electrodes, one that induces feeding and one that induces mating. There are two response levers in the test cage, one for self-stimulation and one for escape from automatic stimulation. With the feeding electrode, rats self-stimulated less and escaped more after a meal than before. The same shift occurred after an anorectic dose of insulin or the commercial appetite suppressant phenylpropanolamine. With the sex electrode the shift from reward to aversion occurred after ejaculation. The review ends with credit to James Olds for pioneering this line of research into the neuropsychology of reinforcement.
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PMID:Hypothalamic self-stimulation and stimulation escape in relation to feeding and mating. 38 51

This study was designed to examine insulin- and exercise-stimulated glucose uptake and metabolism in the hindlimb muscles of rats after conditions of simulated microgravity. To simulate microgravity, male Sprague-Dawley rats were suspended in a head-down (45 degrees) position with their hindlimbs non-weight bearing (SUS) for 14 days. In addition, rats were assigned to suspension followed by exercise (SUS-E), to cage control (CC), or to exercising control (CC-E) groups. Exercise consisted of five 10-min bouts of treadmill running at the same relative intensity for the CC-E and SUS-E rats (80-90% of maximum O2 consumption). Hindlimb perfusion results indicated that glucose uptake for the entire hindquarter at 24,000 microU/ml insulin (maximum stimulation) was significantly higher in the SUS (8.9 +/- 0.5 mumol.g-1.h-1) than in the CC (7.6 +/- 0.4 mumol.g-1.h-1) rats, signifying an increased insulin responsiveness. Glucose uptake at 90 microU/ml insulin was also significantly higher in the SUS (48 +/- 4; % of maximum stimulation over basal) than in the CC (21 +/- 4%) rats. In addition, exercise-induced increases in glucose uptake for the hindlimbs (133%) and glucose incorporation into glycogen for the plantaris (8.4-fold), extensor digitorum longus (5.4-fold), and white gastrocnemius (4.8-fold) muscles were greater for the SUS-E rats than for the CC-E rats (39% and 1.9-, 1.9-, and 3.0-fold, respectively). Therefore, suspension of the rat with hindlimbs non-weight bearing leads to enhanced muscle responses to insulin and exercise when they were applied separately. However, insulin action appeared to be impaired after exercise for the SUS-E rats, especially for the soleus muscle.
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PMID:Effects of insulin and exercise on rat hindlimb muscles after simulated microgravity. 147 84

The IIM are a heterogeneous group of systemic rheumatic diseases which share the common features of chronic muscle weakness and mononuclear cell infiltrates in muscle. A number of classification schemes have been proposed for them, but none takes into consideration the marked immunologic, clinical, and genetic heterogeneity of the various clinical groups. We compared the usefulness of myositis-specific autoantibodies (anti-aminoacyl-tRNA synthetases, anti-SRP, anti-Mi-2 and anti-MAS) to the standard clinical categories (polymyositis, dermatomyositis, overlap myositis, cancer-associated myositis, and inclusion body myositis) in predicting clinical signs and symptoms, HLA types, and prognosis in 212 adult IIM patients. Although patients with inclusion body myositis (n = 26) differed in having significantly more asymmetric and distal weakness, falling, and atrophy than other patients, there were few other significant differences among the other clinical groups. In contrast, autoantibody status defined distinct sets of patients and each patient had only 1 myositis-specific autoantibody. Patients with anti-amino-acyl-tRNA synthetase autoantibodies (n = 47), compared to those without these antibodies, had significantly more frequent arthritis, fever, interstitial lung disease, and "mechanic's hands"; HLA-DRw52; higher mean prednisone dose at survey, higher proportion of patients receiving cytotoxic drugs, and higher death rates. Those with anti-signal recognition particle antibodies (n = 7) had increased palpitations; myalgias; DR5, DRw52; severe, refractory disease; and higher death rates. Patients with anti-Mi-2 antibodies (n = 10) had increased "V-sign" and "shawl-sign" rashes, and cuticular overgrowth; DR7 and DRw53; and a good response to therapy. The 2 patients with anti-MAS antibodies were the only ones with alcoholic rhabdomyolysis preceding myositis; both had insulin-dependent diabetes mellitus, and both had HLA-B60, -C3, -DR4, and -DRw53. These findings suggest that myositis-specific autoantibody status is a more useful guide than clinical group in assessing patients with myositis, and that specific associations of immunogenetics, immune responses, and clinical manifestations occur in IIM. Thus the myositis-specific autoantibodies aid in interpreting the diverse symptoms and signs of myositis patients and in predicting their clinical course and prognosis. We propose, therefore, that an adjunct classification of the IIM, based on the myositis-specific autoantibody status, be incorporated into future studies of their epidemiology, etiology, and therapy.
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PMID:A new approach to the classification of idiopathic inflammatory myopathy: myositis-specific autoantibodies define useful homogeneous patient groups. 165 47

We hypothesized that differential housing, shown to influence emotionality and health in infectious and neoplastic disease, would influence onset/incidence of diabetes in an autoimmune animal model of insulin-dependent diabetes mellitus (IDDM). Non-obese diabetic mice were assigned to same-sex groups of one, five, or eight animals/cage, counterbalanced across shelf level by sex and group. During weekly urine glucose testing, presence of behaviors indicating emotional arousal was recorded. Sex, group, and shelf level affected emotionality: males, animals housed alone, and those on the top of the rack exhibited higher emotionality. Emotionality and shelf level predicted IDDM in females only. Delayed onset of IDDM was associated with high emotionality and with being housed on the top of the rack. Group size had no significant effect on IDDM. Emotionality may be a mediating factor in animals genetically predisposed to develop IDDM. This variable and cage shelf level should be incorporated into the design of studies in which IDDM is the outcome.
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PMID:Group size, cage shelf level, and emotionality in non-obese diabetic mice: impact on onset and incidence of IDDM. 188 12

Previous experiments in which insulin was administered in a Pavlovian conditioning procedure obtained both hyperglycemic and hypoglycemic conditioned responses (CRs). In the present experiment the relationship of the conditioning context and the housing environment was varied. Two environments, wastebasket (WB) and metal cage (MC), were varied factorially as housing and conditioning contexts. Subgroups were injected with either insulin or saline for 6 days and then, on a test day for conditioning, all animals were administered saline. The results suggested that a hyperglycemic CR could be expected when the conditioning context is different from the housing context, but a hypoglycemic CR could be expected when the conditioning context and housing context are similar. The magnitude and reliability of conditioning were greater when it was conducted in the WB context than when conditioning was conducted in the MC context. These results are discussed in terms of stress arising from relative novelty of the conditioning environment and in terms of the salience of the conditioned stimulus (CS) used in glycemic conditioning studies.
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PMID:Relative novelty of conditioning context influences directionality of glycemic conditioning. 257 11

We examined whether chronic exercise prevents insulin resistance developing in the high-fat-fed (HFF) rat, a model that otherwise develops profound peripheral insulin resistance. Insulin action (euglycemic clamp plus 2-[3H]deoxy-D-glucose-[14C]glucose tracer technique) was examined after 3 wk in sedentary control and sedentary or wheel cage exercise-trained HFF rats. At the whole body level, a reduction in peripheral insulin potency in HFF rats was prevented by concomitant chronic exercise; the 30-40% reduction in insulin-stimulated whole body net glucose utilization in sedentary HFF rats was abolished. Responses in individual muscles, however, suggested that the chronic exercise effect may be a compensation for, rather than a correction of insulin resistance induced by a high-fat diet; in six of eight muscles examined it produced an upward additive shift rather than a left shift in insulin dose response. Chronic exercise increased both muscle glycolytic flux and glycogen storage rates in the HFF rats, suggesting that glucose transport may be involved. We conclude that increased physical activity is beneficial in counteracting high-fat diet-induced insulin resistance. Different processes appear to be involved in the development of diet-induced insulin resistance in muscle and its amelioration by regular exercise.
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PMID:Chronic exercise compensates for insulin resistance induced by a high-fat diet in rats. 264 85

The purpose of this study was to assess the effects of chronic insulin infusion on blood pressure and urinary sodium excretion in Wistar rats. Fifteen Male Wistar rats weighing about 220 g were used. The rats were housed in metabolic cage and measured urine volume. Osmotic minipumps filled with insulin (0.57 U/day, Insulin group, n = 9) or saline (0.014 cc/day, Control group, n = 6) were implanted subcutaneously under ether anaesthesia, and blood pressure, urine volume, urinary sodium excretion (UNaV), plasma renin activity (PRA), plasma norepinephrine concentration (PNE) were measured for 4 weeks. In insulin group, there were no significant changes on plasma glucose levels, but systolic blood pressure rose significantly from 119 mmHg to 140 mmHg after 4 weeks. In this group, urine volume, UNaV, and PRA were significantly lower than those of control group and PNE was tended higher but not significant (P less than 0.1). Exogenous NE was given intravenously to assess the endogenous NE activity. Blood pressure elevation caused by exogenous NE in insulin group was suppressed significantly than that of control group. On the basis of these findings, we conclude that insulin can cause high blood pressure due to sodium retention and activation of endogenous NE.
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PMID:[Insulin and hypertension--the mechanisms of high blood pressure during chronic insulin infusion]. 268 19

1. Male rats (110-140 g body wt.) were restrained by a standard laboratory technique, by wrapping in a linen towel, and subjected to a constant intravenous infusion of saline (0.15 M-NaCl) for periods of 1 or 6 h. Fractional rates of protein synthesis (ks, %/day) were estimated at the start and at the end of the infusion period, by injection of a large concentration of [3H]phenylalanine. 2. In fed and overnight-fasted rats, restraint and infusion of saline for 1 and 6 h decreased ks in skeletal muscle by 15-20% and 30-35% respectively. Plasma glucose, insulin, glucagon and corticosterone concentrations in restrained and infused rats were not characteristic of immobilization stress. 3. Restrained rats responded to nutrient administration; ks in skeletal muscle increased by 35-40% after infusion of a mixture of amino acids and glucose for 1 or 6 h, as compared with saline-infused rats. 4. Restraint and infusion for 1 or 6 h did not overtly decrease ks and kRNA (protein synthesis per unit of RNA) in hypoxaemia-sensitive tissues, such as heart and liver. Restraint and infusion in an open cage, or in a cloth of open weave, did not decrease ks in muscle after 1 h. Blood gas measurements showed that rats restrained in a linen cloth were hypercapnic and acidotic compared with rats in an open cage. 5. It was concluded that respiratory acidosis, rather than hypoxia, resulting from restraint in a linen cloth decreases muscle protein synthesis.
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PMID:The influence of restraint and infusion on rates of muscle protein synthesis in the rat. Effect of altered respiratory function. 313 2

Cancer cachexia describes a syndrome of progressive weight loss, anorexia, and persistent erosion of host body cell mass in response to a malignant growth. Although often associated with preterminal patients bearing disseminated disease, cachexia may be present in the early stages of tumor growth before any signs or symptoms of malignancy. A decline in food intake relative to energy expenditure (which may be increased, normal, or decreased) is the fundamental physiologic derangement leading to cancer-associated weight loss. In addition, abnormalities of host carbohydrate, protein, and fat metabolism lead to continued mobilization and ineffective repletion of host tissue, despite adequate nutritional support. Mediators of cancer anorexia and associated abnormalities are unknown. Cachectin/TNF or other host-derived cytokines (produced as a defense against malignancy) have been implicated as signal molecules in cachexia, based upon similar metabolic derangements produced by these cytokines in other chronic wasting illnesses. Nutritional support is effective in maintaining body weight of cachectic cancer patients, but ineffective in maintaining lean body mass. Although in one study parenteral nutritional support has improved operative morbidity and mortality in cancer patients, it has not yet improved response to chemotherapy or radiation therapy. Because of metabolic derangements seen in cancer cachexia, effective nutritional treatment regimens will probably require manipulation of host intermediary metabolism in addition to feeding. Insulin therapy or exercise are two such methods which appear to preserve host composition by preferential feeding of the host at the expense of the tumor. Future studies which more clearly define the role of signal molecules in producing cancer cachexia syndrome may lead to new treatment strategies, possibly involving modulation of the effects of such molecules on host metabolism.
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PMID:Cancer cachexia. 329 98

The effect of physical training on insulin and glucagon release in perfused rat pancreas was examined in the spontaneously exercised group running in a wheel cage an average of 1.4 km/day for 3 weeks and in the sedentary control group kept in the cage whose rotatory wheel was fixed on purpose. Pancreatic immunoreactive insulin (IRI) responses to glucose and arginine were reduced by 28% and 47.8% respectively in trained rats compared with untrained rats, while IRI content of the pancreas was similar in these two groups. The demonstrated decrease in insulin secretion of the beta-cell of the trained rats, in response to the glucose and arginine stimulations, may be functional in nature. On the other hand, neither pancreatic glucagon immunoreactivity (GI) response to glucose and arginine nor GI content of the pancreas was modified by exercise training. These results demonstrate that exercise training reduces IRI responses to glucose as well as to arginine stimulations, but does not modify any secretory response of pancreatic GI.
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PMID:Effect of exercise training on insulin and glucagon release from perfused rat pancreas. 331 58


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