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K A Kern

Publications and source records attributed to K A Kern.

44 records · Page 3Linked to original sources
PubMed1983

Albumin turnover in sarcoma-bearing rats in relation to cancer anorexia.

Hypoalbuminemia, a frequent finding in cancer patients, can be demonstrated in the tumor-bearing rat. In actuality, the circulating amount of albumin is maintained in tumor-bearing rats, although total body water and plasma volume are increased. The fractional degradation rate of newly synthesized albumin labelled by the injection of carbon-14-carbonate was significantly increased in tumor-bearing rats (half-life 55 hours) as compared with control rats (half-life 85 hours). These findings indicate maintained synthesis of albumin in the tumor-bearing rats, a finding consistent with an increased ratio of specific activity in albumin to that in plasma urea after the injection of carbon-14-carbonate. Hypoalbuminemia in cancer seems to be the net result of an increased turnover rate of albumin and dilution of the maintained albumin mass. Despite the presence of cancer anorexia, the flux of substrates from the degradation of peripheral tissues is sufficient to supply the liver and, in turn, to enable an increased protein synthesis with maintenance of the synthetic rate of albumin.

Albumins↗
PubMed1982

The effect of a new branched chain--enriched amino acid solution on postoperative catabolism.

Branched-chain amino acids (BCAAs) may regulate muscle amino acid flux. Metabolic studies of both experimental animals and humans utilizing comparatively large amounts of BCAAs infused with hypocaloric glucose have shown that catabolism and proteolysis can be blunted. These studies suggested that the nitrogen-sparing properties of amino acid solutions used in postoperative trauma or sepsis might be improved by increasing the amount of BCAAs. This hypothesis was tested on ten patients undergoing operations of moderate severity utilizing a peripheral amino acid mixture with a branched-chain:non-branched-chain ratio of 45:55% given in 5% dextrose. The patients received 1.7 gm of protein equivalent/kg of ideal body weight in 5% dextrose-crystalloid solution with a concentration of 3.5% amino acids for the first 5 postoperative days. Nitrogen balance, 3-methylhistidine excretion, blood chemistries, and plasma amino acid profile tests were done daily. The results showed that nitrogen equilibrium was maintained for 5 postoperative days without any untoward effects on patients, their surgical wounds, or hepatic function. Plasma amino acids showed no significant changes from baseline with the exception of elevations of the BCAAs. We conclude that this 45% BCAA-enriched solution may be safely administered to patients with postoperative traumatic injury and results in nitrogen equilibrium over a 5-day period.

Adolescent↗
PubMedDate not supplied

Cancer cachexia.

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.

Anorexia↗