Fat Absorption During Inhibition of Protein Synthesis: Studies of Lymph Chylomicrons

Glickman, Robert M.; Kirsch, Katharina; Isselbacher, Kurt J.

doi:10.1172/jci106821

Cited by 66 publications

(25 citation statements)

References 17 publications

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“…the enterocytes involved were characterized by their low natural capacity to synthesize lipoproteins and to export them. It should also be mentioned that experimental inhibition of protein synthesis in mammals results m an enlargement of enterocytic chylomicrons (Glickman et al 1972) and to extensive development of l~p i d droplets (Sabesin & Isselbacher 1965, Friedman & Cardell 1972.…”

Section: Discussionmentioning

confidence: 99%

Intestinal steatosis in the farm-reared sea bass Dicentrarchus labrax

Deplano¹,

Connes²,

Diaz³

et al. 1989

Dis. Aquat. Org.

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Light microscopy, scanning and transmission electron microscopy were used to study the anterior intestine of the sea bass Dicentrarchus labrax L., involved in lipid absorption. In the first part of the study, intestinal morphology of control feral fishes was described and lipid absorption through the intestinal mucosa was defined by comparing starved and fed individuals. In the second part, similar investigations were made on specimens reared on artificial food. These show injuries of the mucosa, ranging from simple impairment of enterocytic striated border to cellular necrosis and abrasion. The severity of injuries was related to the extent of lipid overloading within the mucosa. This overloadng was mainly represented by abundant lipid droplets in epithelial cells, and by the accumulation of numerous and large lipid granules in interenterocytic spaces and in the lamina propria. Possible influences of artificial feed on this digestive pathology are discussed from quantitative and qualitative points of view.

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Section: Discussionmentioning

confidence: 99%

Intestinal steatosis in the farm-reared sea bass Dicentrarchus labrax

Deplano¹,

Connes²,

Diaz³

et al. 1989

Dis. Aquat. Org.

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“…All animals were fed commercial rat chow (Ziegler Brothers, Inc., Gardners, Pa.) to which they had free access. Cannulation of the main mesenteric lymphatic duct and duodenum was performed as described (13). An exteriorized catheter connecting the common duct to the duodenum was placed as described by Ockner et al (1) and diverted pancreato-biliary secretions.…”

Section: Methodsmentioning

confidence: 99%

Effect of Biliary Diversion on Rat Mesenteric Lymph Apolipoprotein-I and High Density Lipoprotein

Bearnot¹,

Glickman²,

Weinberg³

et al. 1982

J. Clin. Invest.

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A B S T R A C T The effect of biliary diversion on intestinal apolipoprotein (apoA)-I and high density lipoprotein formation was studied in mesenteric lymph fistula rats. Bile diversion was produced by an exteriorized catheter that allowed interruption and reconstitution of the enterohepatic circulation. Bile diversion reduced lymph cholesterol output from 0.47 ± 0.05,umol/h to 0.17 ±0.03Amol/h (P < 0.025), and lymph triglyceride output from 3.6 ± 0.3Stmol/h to 0.6 ± 0.05 ,umol/h (P < 0.025) after 24 h. This was due to depletion of lymph chylomicrons and very low density lipoprotein (VLDL). Despite the reduced lipid outputs, lymph apoA-I output was maintained during biliary diversion (basal: 119 ± 15,gg/h; diverted 140 ± 20,ug/ h, n = 12). During biliary diversion, high density lipoprotein (HDL) were maintained in mesenteric lymph as shown by lipoprotein and immunoelectrophoresis. Bile diversion altered the lipid composition of lymph HDL. Bile-diverted lymph HDL was depleted in total cholesterol and has a greater phospholipid/cholesterol ester ratio than basal lymph HDL. Lymph HDL contained discoidal particles when examined by negative stain electron microscopy. Bile diversion was associated with a reduction in the size of discoidal HDL particles (basal, nondiverted, 165 ± 7A (n = 112) compared with diverted 126±5A (n = 98, P < 0.025).Experiments were then carried out to determine the source of the apoA-I and HDL found in lymph from bile-diverted animals. The transfer of HDL from plasma into lymph was determined by the intravenous infusion of 1251-apoA-I labeled HDL into lymph fistula rats. In both nonbile-diverted and diverted rats, the specific activity of apoA-I in the HDL fraction of lymph was 23% of the specific activity of apoA-I in plasma HDL, indicating that the major portion (75%) of mesenteric lymph apoA-I did not come from plasma filtration. In other experiments the intraduodenal inAddress reprint requests to Dr. Glickman.

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“…The main inhibitors that have been used are puromycin (Redgrave and Zilversmit, 1969 ;Kayden and Medick, 1969 ;Allen et al, 1971 ;Friedman and Cardell, 1972 ;Yousef and Kuksis, 1972 ;Vahouny et al, 1977) and cycloheximide (Sabesin and Isselbacher, Glickman et al, 1970, 1973, 1978 (Glickman et al, 1972 ;Bernard et al, 1980a). Puromycin also caused biochemical changes in esterification or in lymphatic absorption during intestinal lipid absorption (Kayden and Medick, 1969 ;Redgrave and Zilversmit, 1969 ;Yousef and Kuksis, 1972 ;Vahouny et al, 1977 ;Bernard et al, 1980a) ; these perturbations paralleled ultrastructural changes induced by cycloheximide during the same process (Friedman and Cardell, 1972 318 mCi/mmole) 3 1/2 or 4 h after the onset of the inhibitor treatment.…”

mentioning

confidence: 99%

“…Not only is the incorporation of the protein necessary for the formation of chylomicrons and VLDL affected (Glickman et al, 1972), but the processes of esterification are deeply influenced (Bernard et a/., 1980a) and membrane renewal is impaired. According to Friedman and Cardell (1977), it is the preexistent RER in fasted cells that determines good lipid absorption.…”

mentioning

confidence: 99%

“…The considerable diminution in the microvillous absorptive surface, compared to controls (Anderson and Taylor, 1973), already reported in chickens (Lecount and Grey, 1972), explains the lower uptake of lipids by absorptive cells (Bernard et al, 1980a ;Carlier, 1981b, 1983 (Bernard and Carlier, 1980), as well as the aspect of the cellular interdigitations (Altmann, 1975), indicate that the cytoskeleton was affected. These observations provide arguments to explain the defective formation and secretion of lipoprotein particles (Vodovar et al, 1968(Vodovar et al, , 1969Glickman et al, 1972 ;Dobbins, 1966 (Friedman and Cardell, 1977 (1974,1975 …”

mentioning

confidence: 99%

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