Showing papers by "Rosalyn S. Yalow published in 1983"
TL;DR: The brain, unlike the gut, appears to cleave CCK8 rapidly from a precursor peptide but to process the NH2-terminal portions of the molecule more slowly and incompletely.
Abstract: A sequential method employing methanol extraction of the COOH-terminal fragment of cholecystokinin (CCK) from pig brain followed by HCl extraction of the more basic CCK peptides was used as the first step in purification of these peptides. Recovery was monitored with two different assays, one directed to the COOH terminus of CCK and the other to the NH2 terminus. The amino acid content and sequence were determined for each of five peptides after purification. The only peptide containing COOH-terminal immunoreactivity was CCK-octapeptide (CCK8). The other four peptides did not contain CCK8 and had lost one or two additional amino acids, perhaps as a consequence of the action of carboxypeptidases. These peptides were shown to be CCK33-desnonapeptide, CCK39-desnonapeptide and -desdecapeptide, and a large molecular weight precursor, CCK58-desnonapeptide, containing 19 amino acids (Ala-Val-Gln-Lys-Val-Asp-Gly-Glu-Ser-Arg-Ala-His-Leu-Gly-Ala-Leu-Leu-Ala-Arg) NH2-terminal to CCK39. The three NH2-terminal fragments of CCK58, CCK39, and CCK33 were about equally prominent. The brain, unlike the gut, appears to cleave CCK8 rapidly from a precursor peptide but to process the NH2-terminal portions of the molecule more slowly and incompletely.
68 citations
TL;DR: It is concluded that in rat neural tissues, peptide concentrations increase continuously until about 4 weeks, and Gut iCCK peaks at about 2 weeks, presumably due to concentrations increasing in the former and decreasing in the latter tissues.
50 citations
TL;DR: The absence of mechanisms in nonendocrine cells for the complex processing of insulin precursors to the 6000-dalton peptide and the absence of proinsulin in the extracts of the variety of tissues reported from the NIH laboratory suggest that the insulin found in these extracts was ultimately derived from pancreatic insulin.
Abstract: Publisher Summary This chapter provides an overview of insulin in the central nervous system (CNS). Immunohistochemical studies have been employed to visualize the localization of peptide hormones in the brain and other tissues. Before hypothesizing synthesis of insulin in nonpancreatic tissues, one must determine with some accuracy the insulin concentrations in tissues such as the brain of various species or in IM-9 lymphocytes, or of non-guinea pig insulin in guinea pig tissues. If the concentrations are no more than a few percentage points of the levels initially reported by the NIH laboratory, then some explanation should be given for the erroneously high concentrations that were earlier reported. The absence of mechanisms in nonendocrine cells for the complex processing of insulin precursors to the 6000-dalton peptide and the absence of proinsulin in the extracts of the variety of tissues reported from the NIH laboratory suggest that the insulin found in these extracts was ultimately derived from pancreatic insulin.
38 citations
TL;DR: The observations by Della-Fera et al. (1981) that lateral ventricular infusion into sheep of antibody to CCK results in increased feeding is the strongest evidence for a CSF-mediated role for CCK peptides in the regulation of satiety.
Abstract: Publisher Summary This chapter presents the role of CCK-like peptides in appetite regulation. The very high concentrations of CCK peptides in the brain is not consistent with transfer of the peptides from the periphery and, thus, is consistent with CCK synthesis in neuronal and in gut mucosal tissues. Immunohistochemical studies are required to define the cellular elements within the brain that contain CCK immunoreactivity. The chapter discusses the physiological dose levels for the classically defined functions of CCK peptides, that is, their effect on gall bladder contraction and release of pancreatic enzymes. However, the effects of peripheral administration of these peptides on regulation of satiety are achieved only at levels greatly in excess of the physiological range achieved in response to feeding. Thus, endogenous peripheral CCK alone would appear not to be the physiological satiety factor.
6 citations
TL;DR: It is recommended that funding for research in this field be withdrawn until better tools become available - if they ever do - and that a cost-benefit analysis be required prior to any new regulatory decisions.
Abstract: It is well known that acute exposure to high radiation doses can kill in days and that chronic exposure to more moderate doses also may have fatal consequences. It is evident that exposure to low levels of natural radiation has not proven to be harmful. The question addressed is how low is low or are there levels of radiation below which harmful effects cannot be discussed. It is recommended that funding for research in this field be withdrawn until better tools become available - if they ever do - and that a cost-benefit analysis be required prior to any new regulatory decisions.
6 citations