Hydrogel‐based 3D bioprints repair rat small intestine injuries and integrate into native intestinal tissue

Differences in uptake and esterification of saturated analogues of cholesterol by rat small intestine

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1986.251.4.g495 ◽

1986 ◽

Vol 251 (4) ◽

pp. G495-G500 ◽

Cited By ~ 2

Author(s):

A. K. Bhattacharyya

Keyword(s):

Small Intestine ◽

Intestinal Mucosa ◽

Cholesterol Content ◽

Cell Uptake ◽

Cholesterol Concentration ◽

Mucosal Cell ◽

Rat Small Intestine ◽

Intestinal Tissue

Coprostanol and cholestanol are two saturated analogues of cholesterol. The former, which is the A/B ring isomer of cholesterol, is a nonabsorbable sterol, whereas the latter, which has an A/B ring configuration closer to that of cholesterol, is absorbed only half as efficiently as cholesterol. Intestinal mucosal cell uptake and esterification, two important steps in absorption, were studied in vivo after feeding the sterols and in vitro using everted sacs of rat small intestine. The results showed that the intestinal tissue content of coprostanol, total and esterified, were significantly lower than that of cholestanol. Total cholesterol concentration in the intestinal tissue was similar throughout but the esterified cholesterol content increased significantly throughout the length of the intestine compared with controls. The study suggests that cholestanol is absorbable because its uptake and esterification are not limited, whereas coprostanol is nonabsorbable because its uptake and esterification are limited in the intestinal mucosa. Also, the two sterols stimulate the activities of cholesterol esterase, one of the cholesterol esterifying enzymes, in the intestinal mucosa. The present study along with previous studies suggests that the structure of the sterol molecule as a whole appears to be the important determinant for its uptake and esterification, and probably absorption, in the small intestine.

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Specificity studies on enteropeptidase substrates related to the N-terminus of trypsinogen

Biochemical Journal ◽

10.1042/bj2410721 ◽

1987 ◽

Vol 241 (3) ◽

pp. 721-727 ◽

Cited By ~ 3

Author(s):

P Jenö ◽

J R Green ◽

M J Lentze

Keyword(s):

Small Intestine ◽

Methyl Ester ◽

Rat Small Intestine ◽

Concerted Action ◽

Intestinal Tissue ◽

Alternative Substrates ◽

Synthetic Substrate ◽

Highly Active ◽

N Terminus ◽

Aminopeptidase A

The specificity of the synthetic substrate Gly-[L-Asp]4-L-Lys 2-naphthylamide originally developed for the assay of enteropeptidase (EC 3.4.21.9), was investigated with partially purified aminopeptidase. Our results indicate that, not only enteropeptidase, but also the concerted action of the aminopeptidases of the rat small intestine, can rapidly release 2-naphthylamine from the substrate. A previously undescribed, highly active, dipeptidylaminopeptidase, which hydrolyses a Gly-Asp dipeptide from the N-terminus of the substrate, was detected in rat small intestine. The resulting [L-Asp]3-L-Lys 2-naphthylamide fragment is then degraded by a combination of aminopeptidase A and N to yield free 2-naphthylamine. Thus the present substrate cannot be regarded as being specific for enteropeptidase, and its use leads to an over-estimation of enteropeptidase activity in homogenates and extracts of intestinal tissue. In order to prevent this non-specific hydrolysis by aminopeptidases, stereoisomeric substrates with the sequence L-Ala-D-Asp-[L-Asp]3-L-Lys methyl ester, D-Ala-[L-Asp]4-L-Lys methyl ester and L-Ala-[Asp]4-L-Lys methyl ester were synthesized and tested as alternative substrates by their ability to inhibit the enteropeptidase-catalysed activation of trypsinogen.

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Intestinal tissue PO2 and microvascular responses during glucose exposure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1980.238.2.h164 ◽

1980 ◽

Vol 238 (2) ◽

pp. H164-H171 ◽

Cited By ~ 11

Author(s):

H. G. Bohlen

Keyword(s):

Blood Flow ◽

Small Intestine ◽

Normal Distribution ◽

Vascular Resistance ◽

Intestinal Blood Flow ◽

Rat Small Intestine ◽

Intestinal Tissue ◽

Tissue Po2 ◽

In Series ◽

Glucose Exposure

The microvessels responsible for the major decrease in intestinal vascular resistance during the presence of glucose were defined. In addition, the normal distribution of tissue PO2 in the various layers of the intestinal tissue was measured at rest and during glucose exposure to determine if part of the absorptive hyperemia mechanism is related to a decrease in tissue PO2. In the rat small intestine, exposure of the mucosa only to glucose concentrations of 25--500 mg/100 causes a 20--25% dilation of all submucosal vessels in series with the mucosal vessels and mucosal arterioles. Total intestinal blood flow increased to 200-210% of control at all glucose concentrations. The tissue and perivascular PO2 in the villus apex decreased from 14.8 +/- 1.2 (SE) mmHg at rest to 6--8 mmHg during glucose exposure; the PO2 in the muscle and submucosal layers tended to slightly increase above a normal of 26.4 +/- 1.6 mmHg during glucose exposure. The data indicate virtually all intestinal arterioles are equally involved in absorptive hyperemia. The dilation of mucosal vessels may be related to a decrease in tissue PO2, but submucosal vessels dilate even though PO2 is slightly increased.

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