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Biomedical subjects

F S Zhang

Publications and source records attributed to F S Zhang.

14 recordsLinked to original sources
PubMed1991

Anorexia following the intrahypothalamic administration of amylin.

The intrahypothalamic injection of rat amylin reduced feeding in schedule-fed rats for eight hours. Specificity of this anorectic response was indicated by an appropriate dose-response relationship and the absence of effect of human amylin. Amylin-induced anorexia was accompanied by alterations in neurotransmitter metabolism similar to those observed in anorectic tumor-bearing rats. These results indicate that amylin may inhibit feeding by acting directly on hypothalamic neurons to alter metabolism of neurotransmitter systems known to affect feeding behavior.

Amyloid↗
PubMed1991

Lipid-free total parenteral nutrition and macrophage function in rats.

Certain lipids are immunosuppressive when used for nutritional support, while other lipids and nutritional additives may enhance immunologic function. We hypothesized that total parenteral nutrition (TPN) may be immunosuppressive irrespective of lipids. Twenty-four rats underwent central vein catheterization and received either intravenous saline solution and oral chow or TPN alone. At 7 or 14 days, the animals were killed. Splenic and bone marrow macrophages were isolated and cultured in either M199 medium alone or were stimulated with Escherichia coli lipopolysaccharide. The supernatants were tested for prostaglandin E2 and C3. The splenic prostaglandin E2 levels were significantly higher in the TPN group following lipopolysaccharide stimulation at 7 days but not at 14 days. Administration of TPN to rats, even without lipids, may be immunosuppressive through the release of prostaglandin E2 from splenic macrophages following a septic challenge. This effect appears to be abolished after 14 days of TPN infusion.

Animals↗
PubMed1991

Clenbuterol plus acivicin decrease tumor growth and increase muscle mass in rats maintained on total parenteral nutrition.

Two problems associated with supplemental nutrition of tumor-bearing organisms are control of tumor growth and reduction of cachexia. To investigate these problems, rats bearing methylcholanthrene-induced sarcomas were maintained on total parenteral nutrition (TPN) for 10 to 12 days beginning 23 days after tumor inoculation. Combined treatment of one group of these rats with the glutamine antimetabolite, acivicin, and the beta 2-adrenergic agonist, clenbuterol, arrested tumor growth, increased skeletal muscle mass and protein content, increased gut mass, and decreased total plasma lipid levels. Resting energy expenditure and cardiac mass were increased by TPN and were increased further by acivicin plus clenbuterol. These results demonstrate that tumor growth and muscle wasting can be controlled during TPN of tumor-bearing organisms. Therefore, cachectic depletion of lean body tissue may not be obligatory in neoplastic disease.

Animals↗
PubMed1991

Decreased myofibrillar protein breakdown following treatment with clenbuterol.

Daily treatment of Fischer-344 rats for 14 days with the beta 2-adrenergic agonist, clenbuterol, increased gastrocnemius muscle mass and protein content. Coadministration with the beta-adrenergic antagonist, nadolol, significantly reduced these anabolic effects of clenbuterol. Although clenbuterol treatment reduced food intake during the first 4 days, clenbuterol-treated rats were hyperphagic during the second week of drug administration. Nadolol treatment also blocked these effects of clenbuterol on feeding. In a second experiment, in vitro incubation of extensor digitorum longus muscles taken from post weaning food-deprived rats demonstrated decreased release of 3-methylhistidine by clenbuterol-treated rats, suggesting decreased breakdown of myofibrillar protein. Protein synthesis was not increased in vitro in the soleus muscles taken from these rats. These experiments demonstrate that the anabolic effect of clenbuterol is due in part to beta-adrenergic activity and may involve reduced myofibrillar protein degradation. These results appear to have direct application to nutrition and protein repletion in various catabolic diseases.

Adrenergic beta-Antagonists↗
PubMed1991

Methionine sulfoximine intensifies cancer anorexia.

Consistent anorexia was first observed 33 days after inoculating Fischer 344 rats with methylcholanthrene-induced sarcoma. Daily treatment of a similar group of rats with the glutamine synthetase inhibitor, methionine sulfoximine, elicited significant reductions of feeding by day 29 at a dose that had no effect on nontumor-bearing rats. Blood concentrations of ammonia were elevated in both groups of tumor-bearing rats and brain ammonia level was increased in the methionine sulfoximine-treated tumor-bearing rats. Forebrain concentrations of tyrosine, tryptophan, DOPAC and 5-HIAA were elevated in both groups of tumor-bearing rats. Since ammonia is detoxified through the glutamine synthetase reaction, these results suggest that blood and brain ammonia concentrations are more important than the neurochemical consequences of ammonia detoxification for the etiology of cancer anorexia.

Ammonia↗
PubMed1991

Clenbuterol decreases catabolism and increases hypermetabolism in burned rats.

Following a 30% body surface area full-thickness open-flame burn, rats exhibited hypermetabolism, body weight loss, and muscle catabolism. Twenty-one days of treatment of one group of burned rats with the selective beta 2-adrenergic agonist, clenbuterol, increased resting energy expenditure and normalized body weight gain, muscle mass, and muscle protein content. Conversely, similar treatment of another group of burned rats with the long-acting beta-adrenergic antagonist, nadolol, reduced muscle mass, while having no effect on resting energy expenditure, body weight gain, or muscle protein content. These results demonstrate that hypermetabolism does not invariably result in loss of lean body mass and suggest that clenbuterol may be useful in preserving muscle mass and protein in catabolic diseases.

Amino Acids↗
PubMed1991

Reversal of cancer cachexia in rats by cimaterol and supplemental nutrition.

The anabolic beta 2-agonist cimaterol was used in conjunction with supplemental nutrition to reverse cancer-induced cachexia and malnutrition in tumor-bearing rats. Cimaterol was administered to tumor-bearing rats receiving total parenteral nutrition or enteral nutrition for 10 days, beginning 2 weeks after subcutaneous transplantation of methylcholanthrene sarcoma. A significant increase occurred in both muscle weight and muscle protein in animals receiving cimaterol in conjunction with either enteral or parenteral feeding, compared to food fed tumor-bearing animals. Muscle protein content was increased significantly by 16% in cimaterol-treated rats maintained on parenteral nutrition and by 11% in cimaterol-treated enterally fed rats compared with the respective tumor-bearing controls. Urinary concentrations of 3-methylhistidine, an estimation of muscle turnover or catabolism, were significantly reduced in both tumor-bearing groups treated with cimaterol compared to 3-methylhistidine levels of the untreated tumor-bearing groups. The anabolic effects of cimaterol were expressed in the presence of a large tumor burden resulting in reversal of muscle depletion and muscle breakdown regardless of the route of supplemental nutrition. Thus, beta 2-agonists may be considered as a possible therapy for cancer cachexia.

Adrenergic beta-Agonists↗
PubMed1990

Addition of L-glutamine to total parenteral nutrition and its effects on portal insulin and glucagon and the development of hepatic steatosis in rats.

Infusion of total parenteral nutrition (TPN) with excess carbohydrate calories leads to hepatic steatosis in rats and is associated with an elevated portal insulin/glucagon molar ratio. Previously we have shown that adding glucagon to TPN prevents and reverses hepatic steatosis in rats, possibly by increasing hepatic lipid export. It has been reported that steatosis is eliminated in rats by the addition of L-glutamine to TPN. In this study, we examined the effect of glutamine on portal insulin and glucagon levels and the development of hepatic steatosis. Adult rats (n = 19) received internal jugular catheters: Group 1 (n = 6), saline (3 cc/hr) and chow ad libitum; Group 2 (n = 7), 25% dextrose base TPN; Group 3 (n = 6), 25% dextrose base TPN with 2% glutamine. The infusion rate of TPN was 1.2 cc/100 g body wt/hr. Daily nitrogen balance was determined and at 7 days, portal venous blood was drawn for insulin and glucagon radioimmunoassay, livers were removed for histology and lipid content determination, and the small intestines were removed for mucosal protein and DNA content determination. Panlobular vacuolization of the hepatocytes was noted on histology in Group 2 (TPN) while Group 1 (chow) and Group 3 (TPN + glutamine) showed normal liver morphology. Hepatic lipid content was significantly elevated in Group 2 (P less than 0.05). The portal insulin/glucagon molar ratio was increased because of excessive portal venous insulin in Group 2 (TPN). In contrast, portal glucagon was significantly elevated while the insulin/glucagon ratio and hepatic lipid content did not increase above control levels in the glutamine-supplemented Group 3 rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[A quantitative evaluation of rheumatism activity in chronic rheumatic heart disease].

The clinical data of 185 patients with rheumatic heart disease (RHD) proved by pathological biopsies were recorded before operations, and analysed using the stepwise regression analysis of multi-factors (SRAM). A mathematical formula to judge the activities of rheumatism in RHD was applied. The multi-factors were put in order according to their importance in effect: progressive reduction of cardiac function (age less than 30), sustained atrial fibrillation, recent changes in heart murmur or onset of a new murmur, paroxysmal atrial fibrillation, speed-up of erythrocyte sedimentation rate and acute pulmonary edema (age less than 30). 310 cases of RHD were tested and verified by this formula, 85.5% of them were diagnosed correctly in comparison with Aschoff's bodies observed by pathological biopsies in left cardiac atrial appendages. All cases were operated and confirmed by pathological examination. The presence of Aschoff's bodies in atrial appendages was considered the index of active rheumatism pathologically.

Adult↗
PubMed1988

Evaluation of parenteral nutrition in the postoperative patient.

A variety of investigators have attempted to improve nitrogen balance during the postoperative period by modifying the composition of the infused nutrient solutions. This study compared the metabolic effects of administering standard amino acid solutions with a solution enriched with branched chain amino acids (BCAA). A prospective, randomized clinical study was performed in patients who had undergone subtotal gastrectomy or hemicolectomy, and subsequently cared for in the metabolic care unit. The patients were selected from specific entry criteria so that two groups of individuals were comparable. All patients underwent operation without complications. The plasma concentrations of valine and leucine were significantly increased (p less than 0.05 and p less than 0.01, respectively) two days after administration of solutions enriched with BCAA and throughout the entire postoperative period. The plasma glutamine concentrations tended to decrease in both groups; no concentration difference occurred between groups. Nitrogen balance tended to be more positive in the group receiving BCAA but there was no significant difference between groups after operation. Urinary excretion of 3-methylhistidine tended to increase postoperatively in both groups, but no difference occurred between groups. However, the urine excretion of isoleucine increased significantly in the patients receiving infusions enriched with BCAA. Both standard balanced amino acid and amino solutions enriched with BCAA were well tolerated in all patients.

Amino Acids, Branched-Chain↗
PubMedDate not supplied

Clenbuterol treatment increases muscle mass and protein content of tumor-bearing rats maintained on total parenteral nutrition.

Treatment of tumor-bearing (TB) and control rats with the anabolic beta-2 agonist drug clenbuterol (CLE) for 14 days reduced food intake for 4 days initially. Feeding was increased in anorectic TB rats, however, during the last 7 days of drug administration. Since minimal muscle savings were observed in chow-fed TB rats treated with CLE, the anabolic effects of this drug were investigated in a second experiment on TB rats maintained on total parenteral nutrition (TPN). Sixteen days after the subcutaneous transplantation of methylcholanthrene-induced sarcomas rats was begun on a 2-week schedule of TPN. One group of these rats was treated daily for 14 days with CLE, while the remaining rats received injections of saline. Additional groups of TB and nonTB rats were maintained on rat chow for this period and treated with saline. Although TB rats maintained on rat chow or TPN and treated with saline exhibited significantly decreased gastrocnemius muscle weight and protein content, treatment of TB-TPN rats with clenbuterol normalized muscle mass and increased muscle protein content significantly and increased plasma concentrations of branched-chain amino acids. These results indicate that although nutritional support of TB organisms does not result in protein repletion, the addition of an anabolic drug renders the nutritional support highly efficacious.

Animals↗