Robert
Pergolizzi,2
Fima
Lifshitz,3
ABSTRACT
Saul
The
70%
than
controls.
The
levels
intake.
and
decrease
only
diarrhea
fed
were
tural
abnormalities.
ment
was
similar were
disaccharidases diarrhea
but
a glucose
induced
days
not
had
3H-thymidine
show
in height an enhanced
by an osmotic
and
The American
Journal
lactose
with
diarrhea.
led when
rats
of all
appearance.
were
and
sucrase
were
fed
DNA
These
The
cells suggest
that
the corresponding
J. Cliii. Nutr.
in
Deficiencies
in
diet,
while
in intestinal
of mannitol
not
a
mannitol-induced or ultrastructreat-
damaged
and
levels
of specific
the
dietary
30:482-489,
to dietary
cells
7 days were
ad less
deficiencies
changes
of epithelial
following data
with
fed but
related
a sucrose
Rats
disaccharidases.
were
weight,
rats
unchanged.
diet.
epithelial
upon
in rats with
starch
gained
were
in the number into
50%
They
to lactase
phosphatase
Absorptive
Am.
disaccharidases
in mannitol-fed
alterations
dependence load.
jejunal
a lactose-starch
incorporation controls.
The relationship between the intake of carbohydrates (CHO’s) and the levels of intestinal disaccharidases remains to be fully clarified. For example, in rats it has been shown that lactase levels were increased by dietary lactose (1-4), and induction of this enzyme could be achieved by in utero exposure to that sugar (5). Other authors have published conflicting reports on the relationship between disaccharide intake and intestinal disaccharidases, both in rats (6) and humans (7-10). In diarrheal disease, there may be secondary alterations in the intestinal mucosa and some deficiencies in disaccharidase activities (11-14). Thus, the ingestion of disaccharides during the acute stage of illness may lead to increased severity of diarrhea, acidosis, and CHO intolerance (15), which improved following elimination of the offending CHO from the diet (15-18). However, because of the possible relationship between dietary CHO and intestinal disaccharidases, the enzyme deficiencies may be prolonged or even aggravated. Thus, the traditional
482
fed
Wapnir
Weanling rats were force-fed 5 ml/100 mOsm) daily for up to 14 days. Diets
and
induced
levels
with
on
treatment
were
reduced
A.
or 20%
intake
and alkaline
in rats
not associated
to water-fed normal
glucose, water
disaccharidases
in sucrase
occurred diet
intake
of mannitol
jejunal maltase
in sucrase
disaccharidases
microvilli
of intestinal
Seven
maltase
sucrose,
rats had increased
rats fed starch whereas lactase
starch,
Raul
were studied. (w/v 1300
osmotic diarrhea of 20% mannitol
of either
libitum. Mannitol-fed carbohydrate
and
effects of carbohydrate
chronic mannitol-induced, g of body weight of water containing
Teichberg,
substrates
the
during
1977.
method of dietary treatment in diarrhea (19), involving the removal of the offending CHO, may itself give rise to subsequent intestinal enzyme deficiencies. In the present study, on an animal model system, we have focused our attention on the influence of dietary CHO’s on the levels of specific intestinal disaccharidases during mannitol-induced osmotic diarrhea. Our findings suggest that specific dietary CHO intake prevents the decreases in the corresponding jejunal disaccharidase induced by chronic force-feedings of mannitol. Methods
and
Experiments Wistar-derived
materials were CFN
conducted strain
with
(Carworth
male Animal
rats
of
the
Breed-
From the Department of Pediatrics and Laboratories, North Shore University Hospital, Manhasset, New York 11030 and the Department of Pediatrics, Cornell University Medical College, New York, New York 10021. 2 Research Assistant. Address reprint requests to: Dr. Fima Lifshitz, Department of Pediatrics, North Shore University Hospital, Manhasset, New York 11030.
of Clinical Nutrition
30: APRIL
1977,
pp.
482-489.
Printed
in U.S.A.
Downloaded from https://academic.oup.com/ajcn/article-abstract/30/4/482/4650286 by University of Rhode Island user on 08 December 2018
Inte ract ion between d ieta ry ca rbo hyd rates and intestinal disaccharidases in experimental diarrhea1
CARBOHYDRATES
AND
DISSACHARIDASES
IN
EXPERIMENTAL
DIARRHEA
483
TABLE
1 response
The
to hyperosmotic
force-feedings
of mannitol Mannitol’
7.36 66 32.2
PO2 (mm Hg) pCO2 (mm Hg) Plasma HCO3(mEq/liter) Na (mEq/liter) K (mEq/liter) Cl (mEq/liter) Intestine Fluid pH Fluid volume (ml) Weight (g/cm) n 6 rats per group Data
#{176}
are
means
± SEM.
±
Controls
#{216}09b
±
24 ± 12.4
7.41 ± 0.08 81 ± 20 26.1 ± 17.1
19.95 144.5 5.04 108.6
2.09 5.84 ± 0.89 ± 5.44
19.70 142.4 5.25 102.5
±
6.31 2.25 0.047
±
0.30 0.23k’ ± 0.004
6.22 0.37 0.046
±
± ±
±
1.75 8.69 ± 0.55 ± 5.55 ±
0.27 0.20 ± 0.006 ±
< 0.0 5.
ers, Inc.) with mean initial weights of 76 ± 4 g. The rats were randomly divided into experimental and control groups. Diarrhea was induced in the experimental animals by forced feedings of mannitol as follows: 20% (w/v) 1300 mOsm solution of mannitol was given to the experimental groups once daily in the morning, at the dose of 5 ml per 100 g body weight by intragastric instillation. Control rats were force-fed identical amounts of water. Animals were killed and studied after 2 hr, 1, 2, 7, and 14 days of experimental manipulation. The animals were housed in Acme metabolic cages equipped with devices to separate solid stools from urine. Rats were fed ad libitum water and diets containing 70% CHO 8% fat, and 18% protein, plus vitamins and minerals . The following CHOs were given: 1) 70% starch, 2) 70% sucrose, 3) 20% lactose plus 50% starch, and 4) 70% glucose. In some instances rats were pair fed. Body weight, water intake, stool and urine output were all measured daily. Rats given mannitol had diarrhea (total excreta was 11.0 ± 2.0 in mannitol rats versus 4.8 ± 1.1 in controls mi/day respectively), and drank more water (17 ± 2 versus 8 ± 2 mI/day, P < 0.05). The experimental rats gained weight but less than the controls (105 ± 5 versus 119 ± 3 g after 14 days of treatment P
Pergolizzi,2
Fima
Lifshitz,3
ABSTRACT
Saul
The
70%
than
controls.
The
levels
intake.
and
decrease
only
diarrhea
fed
were
tural
abnormalities.
ment
was
similar were
disaccharidases diarrhea
but
a glucose
induced
days
not
had
3H-thymidine
show
in height an enhanced
by an osmotic
and
The American
Journal
lactose
with
diarrhea.
led when
rats
of all
appearance.
were
and
sucrase
were
fed
DNA
These
The
cells suggest
that
the corresponding
J. Cliii. Nutr.
in
Deficiencies
in
diet,
while
in intestinal
of mannitol
not
a
mannitol-induced or ultrastructreat-
damaged
and
levels
of specific
the
dietary
30:482-489,
to dietary
cells
7 days were
ad less
deficiencies
changes
of epithelial
following data
with
fed but
related
a sucrose
Rats
disaccharidases.
were
weight,
rats
unchanged.
diet.
epithelial
upon
in rats with
starch
gained
were
in the number into
50%
They
to lactase
phosphatase
Absorptive
Am.
disaccharidases
in mannitol-fed
alterations
dependence load.
jejunal
a lactose-starch
incorporation controls.
The relationship between the intake of carbohydrates (CHO’s) and the levels of intestinal disaccharidases remains to be fully clarified. For example, in rats it has been shown that lactase levels were increased by dietary lactose (1-4), and induction of this enzyme could be achieved by in utero exposure to that sugar (5). Other authors have published conflicting reports on the relationship between disaccharide intake and intestinal disaccharidases, both in rats (6) and humans (7-10). In diarrheal disease, there may be secondary alterations in the intestinal mucosa and some deficiencies in disaccharidase activities (11-14). Thus, the ingestion of disaccharides during the acute stage of illness may lead to increased severity of diarrhea, acidosis, and CHO intolerance (15), which improved following elimination of the offending CHO from the diet (15-18). However, because of the possible relationship between dietary CHO and intestinal disaccharidases, the enzyme deficiencies may be prolonged or even aggravated. Thus, the traditional
482
fed
Wapnir
Weanling rats were force-fed 5 ml/100 mOsm) daily for up to 14 days. Diets
and
induced
levels
with
on
treatment
were
reduced
A.
or 20%
intake
and alkaline
in rats
not associated
to water-fed normal
glucose, water
disaccharidases
in sucrase
occurred diet
intake
of mannitol
jejunal maltase
in sucrase
disaccharidases
microvilli
of intestinal
Seven
maltase
sucrose,
rats had increased
rats fed starch whereas lactase
starch,
Raul
were studied. (w/v 1300
osmotic diarrhea of 20% mannitol
of either
libitum. Mannitol-fed carbohydrate
and
effects of carbohydrate
chronic mannitol-induced, g of body weight of water containing
Teichberg,
substrates
the
during
1977.
method of dietary treatment in diarrhea (19), involving the removal of the offending CHO, may itself give rise to subsequent intestinal enzyme deficiencies. In the present study, on an animal model system, we have focused our attention on the influence of dietary CHO’s on the levels of specific intestinal disaccharidases during mannitol-induced osmotic diarrhea. Our findings suggest that specific dietary CHO intake prevents the decreases in the corresponding jejunal disaccharidase induced by chronic force-feedings of mannitol. Methods
and
Experiments Wistar-derived
materials were CFN
conducted strain
with
(Carworth
male Animal
rats
of
the
Breed-
From the Department of Pediatrics and Laboratories, North Shore University Hospital, Manhasset, New York 11030 and the Department of Pediatrics, Cornell University Medical College, New York, New York 10021. 2 Research Assistant. Address reprint requests to: Dr. Fima Lifshitz, Department of Pediatrics, North Shore University Hospital, Manhasset, New York 11030.
of Clinical Nutrition
30: APRIL
1977,
pp.
482-489.
Printed
in U.S.A.
Downloaded from https://academic.oup.com/ajcn/article-abstract/30/4/482/4650286 by University of Rhode Island user on 08 December 2018
Inte ract ion between d ieta ry ca rbo hyd rates and intestinal disaccharidases in experimental diarrhea1
CARBOHYDRATES
AND
DISSACHARIDASES
IN
EXPERIMENTAL
DIARRHEA
483
TABLE
1 response
The
to hyperosmotic
force-feedings
of mannitol Mannitol’
7.36 66 32.2
PO2 (mm Hg) pCO2 (mm Hg) Plasma HCO3(mEq/liter) Na (mEq/liter) K (mEq/liter) Cl (mEq/liter) Intestine Fluid pH Fluid volume (ml) Weight (g/cm) n 6 rats per group Data
#{176}
are
means
± SEM.
±
Controls
#{216}09b
±
24 ± 12.4
7.41 ± 0.08 81 ± 20 26.1 ± 17.1
19.95 144.5 5.04 108.6
2.09 5.84 ± 0.89 ± 5.44
19.70 142.4 5.25 102.5
±
6.31 2.25 0.047
±
0.30 0.23k’ ± 0.004
6.22 0.37 0.046
±
± ±
±
1.75 8.69 ± 0.55 ± 5.55 ±
0.27 0.20 ± 0.006 ±
< 0.0 5.
ers, Inc.) with mean initial weights of 76 ± 4 g. The rats were randomly divided into experimental and control groups. Diarrhea was induced in the experimental animals by forced feedings of mannitol as follows: 20% (w/v) 1300 mOsm solution of mannitol was given to the experimental groups once daily in the morning, at the dose of 5 ml per 100 g body weight by intragastric instillation. Control rats were force-fed identical amounts of water. Animals were killed and studied after 2 hr, 1, 2, 7, and 14 days of experimental manipulation. The animals were housed in Acme metabolic cages equipped with devices to separate solid stools from urine. Rats were fed ad libitum water and diets containing 70% CHO 8% fat, and 18% protein, plus vitamins and minerals . The following CHOs were given: 1) 70% starch, 2) 70% sucrose, 3) 20% lactose plus 50% starch, and 4) 70% glucose. In some instances rats were pair fed. Body weight, water intake, stool and urine output were all measured daily. Rats given mannitol had diarrhea (total excreta was 11.0 ± 2.0 in mannitol rats versus 4.8 ± 1.1 in controls mi/day respectively), and drank more water (17 ± 2 versus 8 ± 2 mI/day, P < 0.05). The experimental rats gained weight but less than the controls (105 ± 5 versus 119 ± 3 g after 14 days of treatment P
