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S Mishkin

Publications and source records attributed to S Mishkin.

50 records · Page 3Linked to original sources
PubMed1972

Stages of uptake and incorporation of micellar palmitic acid by hamster proximal intestinal mucosa.

The stages of uptake and incorporation of micellar palmitic acid by hamster proximal intestinal mucosa were investigated by incubation of everted sacs at 4 degrees C and 37 degrees C for 2, 5, 10, and 15 min in a micellar solution (10 micro moles of [1-(14)C]palmitic acid, 10 micro moles of monoolein, and 100 micro moles of sodium taurodeoxycholate) and subsequent serial rinsing of the sacs in ice-cold solutions as follows: one 20-sec rinse in unlabeled micellar solution, five 1-min rinses in Krebs-Ringer buffer (0.15 m, pH 6.3), and ten 2-min rinses in 2.5% albumin solution. The fatty acid-solubilizing capacity of all the rinsing solutions was always in excess of the amounts of radioactive palmitic acid released during each rinse. Radioactivity was determined in the tissue homogenates, rinsing solutions, and serosal fluids. The results indicate that a significant proportion of radioactive palmitic acid taken up by the sacs during the short incubation was released into the rinsing solutions. Rinsing in Krebs-Ringer buffer resulted in release of 15.5 +/- 2.4% of the labeled fatty acid, and this fraction was independent of the temperature of incubation. In contrast, the amounts of palmitic acid released in albumin were significantly greater and were markedly dependent on the temperature of incubation; a total of 48.6 +/- 7.0% and 26.3 +/- 5.1% was released from sacs incubated at 4 degrees C and 37 degrees C, respectively. While the proportion of radioactive palmitic acid in the free fatty acid fraction of the tissue after the rinsing sequence remained reasonably constant regardless of the temperature and duration of incubation, the radioactivity of the esterified palmitic acid in the tissue was much greater in the sacs incubated at 37 degrees C and tended to increase linearly up to 10 min of incubation. A highly significant inverse relationship was found between the fraction of radioactive palmitic acid released by rinsing in albumin and the fraction of the label in the tissue esterified fatty acids. The results suggest that the initial uptake of micellar fatty acid by intestinal mucosa may involve reversible binding to superficial sites with at least two strengths of binding: a weak, temperature-independent binding which could be easily dissociated by rinsing in Krebs-Ringer buffer, and a stronger, temperature-dependent binding which could be dissociated by rinsing in albumin, but not in Krebs-Ringer buffer. Analogous binding of micellar palmitic acid occurred in a brush border preparation of proximal intestine which was devoid of any fatty acid esterifying activity. This suggested that the reversible binding of fatty acid by the intestinal mucosa may be a property of its superficial components, namely the glycocalyx or microvillous membranes, and that it may be independent of the esterifying capacity of the tissue.

Animals↗
PubMed1969

Effect of DL-ethionine on the intestinal absorption and transport of palmitic acid-1-14C and tripalmitin-14C. Role of intramucosal factors in the uptake of luminal lipids.

The effect of DL-ethionine on the uptake and transport of lipid by the rat small intestine was investigated. A cottonseed oil emulsion containing (14)C-labeled tripalmitin or palmitic acid was administered intragastrically to rats pretreated with DL-ethionine, DL-ethionine plus methionine, or saline, and the rats were sacrificed 2, 4, and 6 hr later. Lipids from the plasma, the stomach, the colon, the luminal contents of the small intestine, and the wall of the small intestine were extracted, fractionated, and their radioactivity assayed. Ethionine markedly inhibited the uptake of lipids by the small intestine. This inhibition was not related to impairment of intraluminal lipolysis since analagous inhibitions were observed when palmitic acid or predigested triglyceride (TG), obtained through a jejunal fistula from normal animals, was administered instead of tripalmitin. Ethionine also inhibited the transport of lipid from the wall of the small intestine. A significant fraction of the administered lipid remained in the wall of the small intestine, and only a small fraction was transported to the blood stream. Although most of the wall radioactivity was in the form of TG, significant proportions were also found in the free fatty acid (FFA) and partial glyceride fractions, indicating a marked inhibition of mucosal reesterification to TG. The degree of inhibition of mucosal reesterification and the degree of inhibition of transport of wall lipids were directly related to the degree of inhibition of uptake of luminal radioactivity. This relationship suggests that the rate of reesterification, the level of mucosal FFA, and the rate of transport of intramucosal TG may be of importance in determining the extent of uptake of intraluminal lipid by the mucosal cells. Since a significant fraction of the wall radioactivity was in the form of TG, the decreased transport of wall lipids was attributed to an impairment of chylomicron completion due to inhibition of either the synthesis of chylomicron apoprotein or the association of preformed TG with the protein moiety of chylomicrons. Experiments with labeled amino acids support the first possibility.

Animals↗
PubMedDate not supplied

Evidence for the hormone dependency of hepatic hyperplastic nodules: inhibition of malignant transformation after exogenous 17 beta-estradiol and tamoxifen.

Hepatic hyperplastic nodules (HHNs) in rats were studied as an experimental prototype of oral contraceptive-related hepatic tumors. We have found cytoplasmic estrogen receptors in HHNs produced by acetylaminofluorene (AAF) (four cycles of 0.02% in diet). Rats with AAF-induced HHNs were randomized into four groups: (i) AAF-treated control; (ii) estrogen alone (estradiol-17 beta); (iii) tamoxifen alone, and (iv) estrogen + tamoxifen. After 8 months of treatment with estrogen (estradiol-17 beta) in combination with tamoxifen, there was regression of nodular involvement and no evidence of malignant transformation. Decreased nodular proliferation also occurred after 2 and 4 months treatment with estradiol-17 beta and after 8 months of tamoxifen administration. The incidence of hepatocellular carcinoma after 8 months of treatment was significantly less after treatment with estrogen (40%) or tamoxifen (42.9%) when compared to AAF-treated controls (87.5%). The number of gamma-glutamyltranspeptidase-positive foci were reduced in all treatment groups after 2, 4, and 8 months of treatment; these changes were most pronounced in the estrogen-treated group and did not directly correlate with the per cent inhibition of malignant transformation. Our results suggest that the malignant transformation of estrogen receptor-positive HHNs is hormone dependent.

2-Acetylaminofluorene↗
PubMedDate not supplied

Dietary fads and gut mysteries versus nutrition with a grain of common sense.

Although nutritional self-help literature is directed at the general public, which usually allows the authors to evade critical review by the medical and scientific community, both doctors and lay people need to read with discernment and educated scepticism when major health claims are made. Many published claims are based in misconceptions and questionable logic, and it is important to be aware of the inconsistencies and wrong conclusions commonly found in dietary fads. Patients' questions and dietary practices over the past few years have helped the present authors become familiar with certain food fads and nutrition 'self-help' books, and develop responses to popular gut topics such as food allergies, food combinations and commercial food supplements. The authors also discuss whether fads can deliver on their promises and what to tell patients.

Diet Fads↗