monty1945
Sun, Jun-25-06, 17:15
It's been noted (as insiders already know):
"The protective effect of dietary saturated fatty acids
against the development of alcoholic liver disease has long
been known..."
Source: Hepatology. 2005 Sep;42(3):568-77.
Role of adiponectin in the protective action of dietary
saturated fat against alcoholic fatty liver in mice.
You M, Considine RV, Leone TC, Kelly DP, Crabb DW.
Such studies as the following are common:
Dietary saturated fat reduces alcoholic hepatotoxicity in
rats by altering fatty acid metabolism and membrane
composition.
Ronis MJ, Korourian S, Zipperman M, Hakkak R, Badger TM.
Arkansas Children's Nutrition Center, Department of
Pharmacology/Toxicology, University of Arkansas for
Medical Sciences, Little Rock, AR 72205, USA.
RonisMartin@uams.edu
Rats fed a saturated fat diet are protected from
experimentally induced alcoholic liver disease, but the
molecular mechanisms underlying this phenomenon remain in
dispute. We fed male Sprague-Dawley rats intragastrically
by total enteral nutrition using diets with or without
ethanol. In 1 control and 1 ethanol group, the dietary fat
was corn oil at a level of 45% of total energy. In other
groups, saturated fat [18:82 ratio of beef
tallow:medium-chain triglyceride (MCT) oil] was
substituted for corn oil at levels of 10, 20, and 30% of
total energy, while keeping the total energy from fat at
45%. After 70 d, liver pathology, serum alanine
aminotransferase (ALT), biochemical markers of oxidative
stress, liver fatty acid composition, cytochrome P450 2E1
(CYP2E1) expression and activity and cytochrome P450 4A
(CYP4A) expression were assessed. In rats fed the corn oil
plus ethanol diet, hepatotoxicity was accompanied by
oxidative stress. As dietary saturated fat content
increased, all measures of hepatic pathology and oxidative
stress were progressively reduced, including steatosis (P
< 0.05). Thus, saturated fat protected rats from alcoholic
liver disease in a dose-responsive fashion. Changes in
dietary fat composition did not alter ethanol metabolism
or CYP2E1 induction, but hepatic CYP4A levels increased
markedly in rats fed the saturated fat diet. Dietary
saturated fat also decreased liver triglyceride, PUFA, and
total FFA concentrations (P < 0.05). Increases in dietary
saturated fat increased liver membrane resistance to
oxidative stress. In addition, reduced alcoholic steatosis
was associated with reduced fatty acid synthesis in
combination with increased CYP4A-catalyzed fatty acid
oxidation and effects on lipid export. These findings may
be important in the nutritional management and treatment
of alcoholic liver disease.
In contrast, however:
Free Radic Biol Med. 2002 Jan 1;32(1):38-45.
Lipid peroxidation contributes to immune reactions associated
with alcoholic liver disease.
Mottaran E, Stewart SF, Rolla R, Vay D, Cipriani V, Moretti M,
Vidali M, Sartori M, Rigamonti C, Day CP, Albano E.
Increasing evidence indicates the involvement of immune
reactions in the pathogenesis of alcoholic liver disease. We
have investigated whether ethanol-induced oxidative stress
might contribute to immune response in alcoholics. Antibodies
against human serum albumin modified by reaction with
malondialdehyde (MDA), 4-hydroxynonenal (HNE), 2-hexenal,
acrolein, methylglyoxal, and oxidized arachidonic and linoleic
acids were measured by ELISA in 78 patients with alcoholic
cirrhosis and/or hepatitis, 50 patients with nonalcoholic
cirrhosis, 23 heavy drinkers with fatty liver, and 80
controls. Titers of IgG-recognizing epitopes derived from MDA,
HNE, and oxidized fatty acids were significantly higher in
alcoholic as compared to nonalcoholic cirrhotics or healthy
controls. No differences were instead observed in the titers
of IgG-recognizing acrolein-, 2-hexenal-, and
methylglyoxal-modified albumin. Alcoholics showing high IgG
titers to one adduct tended to have high titers to all the
others. However, competition experiments showed that the
antigens recognized were structurally unrelated. Anti-MDA and
anti-HNE antibodies were significantly higher in cirrhotics
with more severe disease as well as in heavy drinkers with
cirrhosis or extensive fibrosis than in those with fatty liver
only. We conclude that antigens derived from lipid
peroxidation contribute to the development of immune responses
associated with alcoholic liver disease.
Understand the scientfic reality of health and "disease" at:
http://groups.msn.com/TheScientificDebateForum-/
No need to be confused by all the conflicting "studies" the
mainstream media likes to tout (most people don't realize that
for every study the media emphasizes there are hundreds if not
thousands of others on the same subject that have never been
mentioned by them).
"The protective effect of dietary saturated fatty acids
against the development of alcoholic liver disease has long
been known..."
Source: Hepatology. 2005 Sep;42(3):568-77.
Role of adiponectin in the protective action of dietary
saturated fat against alcoholic fatty liver in mice.
You M, Considine RV, Leone TC, Kelly DP, Crabb DW.
Such studies as the following are common:
Dietary saturated fat reduces alcoholic hepatotoxicity in
rats by altering fatty acid metabolism and membrane
composition.
Ronis MJ, Korourian S, Zipperman M, Hakkak R, Badger TM.
Arkansas Children's Nutrition Center, Department of
Pharmacology/Toxicology, University of Arkansas for
Medical Sciences, Little Rock, AR 72205, USA.
RonisMartin@uams.edu
Rats fed a saturated fat diet are protected from
experimentally induced alcoholic liver disease, but the
molecular mechanisms underlying this phenomenon remain in
dispute. We fed male Sprague-Dawley rats intragastrically
by total enteral nutrition using diets with or without
ethanol. In 1 control and 1 ethanol group, the dietary fat
was corn oil at a level of 45% of total energy. In other
groups, saturated fat [18:82 ratio of beef
tallow:medium-chain triglyceride (MCT) oil] was
substituted for corn oil at levels of 10, 20, and 30% of
total energy, while keeping the total energy from fat at
45%. After 70 d, liver pathology, serum alanine
aminotransferase (ALT), biochemical markers of oxidative
stress, liver fatty acid composition, cytochrome P450 2E1
(CYP2E1) expression and activity and cytochrome P450 4A
(CYP4A) expression were assessed. In rats fed the corn oil
plus ethanol diet, hepatotoxicity was accompanied by
oxidative stress. As dietary saturated fat content
increased, all measures of hepatic pathology and oxidative
stress were progressively reduced, including steatosis (P
< 0.05). Thus, saturated fat protected rats from alcoholic
liver disease in a dose-responsive fashion. Changes in
dietary fat composition did not alter ethanol metabolism
or CYP2E1 induction, but hepatic CYP4A levels increased
markedly in rats fed the saturated fat diet. Dietary
saturated fat also decreased liver triglyceride, PUFA, and
total FFA concentrations (P < 0.05). Increases in dietary
saturated fat increased liver membrane resistance to
oxidative stress. In addition, reduced alcoholic steatosis
was associated with reduced fatty acid synthesis in
combination with increased CYP4A-catalyzed fatty acid
oxidation and effects on lipid export. These findings may
be important in the nutritional management and treatment
of alcoholic liver disease.
In contrast, however:
Free Radic Biol Med. 2002 Jan 1;32(1):38-45.
Lipid peroxidation contributes to immune reactions associated
with alcoholic liver disease.
Mottaran E, Stewart SF, Rolla R, Vay D, Cipriani V, Moretti M,
Vidali M, Sartori M, Rigamonti C, Day CP, Albano E.
Increasing evidence indicates the involvement of immune
reactions in the pathogenesis of alcoholic liver disease. We
have investigated whether ethanol-induced oxidative stress
might contribute to immune response in alcoholics. Antibodies
against human serum albumin modified by reaction with
malondialdehyde (MDA), 4-hydroxynonenal (HNE), 2-hexenal,
acrolein, methylglyoxal, and oxidized arachidonic and linoleic
acids were measured by ELISA in 78 patients with alcoholic
cirrhosis and/or hepatitis, 50 patients with nonalcoholic
cirrhosis, 23 heavy drinkers with fatty liver, and 80
controls. Titers of IgG-recognizing epitopes derived from MDA,
HNE, and oxidized fatty acids were significantly higher in
alcoholic as compared to nonalcoholic cirrhotics or healthy
controls. No differences were instead observed in the titers
of IgG-recognizing acrolein-, 2-hexenal-, and
methylglyoxal-modified albumin. Alcoholics showing high IgG
titers to one adduct tended to have high titers to all the
others. However, competition experiments showed that the
antigens recognized were structurally unrelated. Anti-MDA and
anti-HNE antibodies were significantly higher in cirrhotics
with more severe disease as well as in heavy drinkers with
cirrhosis or extensive fibrosis than in those with fatty liver
only. We conclude that antigens derived from lipid
peroxidation contribute to the development of immune responses
associated with alcoholic liver disease.
Understand the scientfic reality of health and "disease" at:
http://groups.msn.com/TheScientificDebateForum-/
No need to be confused by all the conflicting "studies" the
mainstream media likes to tout (most people don't realize that
for every study the media emphasizes there are hundreds if not
thousands of others on the same subject that have never been
mentioned by them).