Effect of Alcohol Consumption on Adult and Aged Bone: Composition, Morphology, and Hormone Levels of a Rat Animal Model

To determine the effect of life-long alcohol consumption on the adult and aged rat model, 4-week-old, female Sprague-Dawley rats were divided into three diet groups. Alcohol-treated animals were fed a modified Lieber-DeCarli diet ad libitum containing 35% ethanol-derived calories, whereas the pair-fed animals (weight-matched to ethanol rats) received an isocaloric liquid diet in which maltose-dextrin substituted calories supplied by ethanol. Chow animals were fed a standard rat chow ad libitum. Proximal tibiae (primarily cancellous bone) and femora (primarily cortical bone) were removed for analysis after 3, 6, 9, 12, or 18 months on the diets. Serum was collected for analysis of calcium levels, the calcium regulating hormones; parathyroid hormone, 25-hydroxyvitamin D, calcitonin, cor-ticosterone, estradiol, testosterone, and IGF-1. Creatinine, SGOT/ AST, and SGPT/ALT levels were measured to determine kidney and liver integrity. Previous studies, with young animals, showed that chronic alcohol consumption during the age of bone development reduced bone density and bone mass in both cortical and cancellous bone. The present study demonstrates that these reductions last throughout life, whereas morphological values, such as length and diameter, attain control levels. Calcium regulating hormones and sex hormones are essentially normal and do not appear to be the primary causative agent for adult alcohol-induced osteopenia, but it appears to be due to a more direct effect of alcohol on bone cells.     

Alcohol Consumption by Young Actively Growing Rats: A Histomorphometric Study of Cancellous Bone

Alcohol consumption by young actively growing rats has been previously demonstrated to decrease bone density. This study addresses the mechanism of alcohol action on the early phases of bone growth and development using histomorphometric techniques. Four-week-old, female Sprague-Dawley rats were divided into three groups. Alcohol-treated animals were fed a modified Lieber-DeCarli diet ad libitum containing 35% ethanol-derived calories, whereas the pair-fed animals (weight-matched to ethanol rats) received an isocaloric liquid diet in which maltose-dextrin-substituted calories were supplied by ethanol. Chow animals were fed a standard rat chow ad libitum. Proximal tibiae, including epiphyseal growth plate, were removed for analysis after 2,4, 6, or 8 weeks on the diets. Trabecular volume and number were greatly reduced in the alcohol-fed animals; however, bone formation rates and mineralization rates were normal. Epiphyseal growth rate and proliferation rate were essentially stopped in the alcohol-fed animals.     

Alcohol Consumption by Young Actively Growing Rats: A Study of Cortical Bone Histomorphometry and Mechanical Properties

Alcohol consumption by young actively growing rats has been previously demonstrated to decrease cortical and cancellous bone density, to reduce trabecular bone volume, and to inhibit bone growth at the epiphyseal growth plate. This study addresses the action of alcohol on cortical bone growth using histomorphometric techniques and on mechanical properties by three-point bending. Four-week-old, female Sprague-Dawley rats were divided into three groups. Alcohol-treated animals were fed a modified Lieber-DeCarli diet ad libitum containing 35% ethanol-derived calories, whereas the pairfed animals (weight-matched to ethanol rats) received an isocaloric liquid diet in which maltose-dextrin-substituted calories were supplied by ethanol. Chow animals were fed a standard rat chow ad libitum. Femora were removed for analysis after 2, 4, 6, or 8 weeks on the diets. Cortical bone area, bone formation rates, and mineral apposition rates were reduced in the alcohol-fed animals. Bone stiffness, strength, and energy absorbed to fracture were significantly lower in the alcohol-fed animals. This distinctive alcohol effect was revealed to be caused by lower quality bone tissue as reflected by lower elastic moduli and yield strengths.     

Alcohol Consumption Inhibits Bone Growth and Development in Young Actively Growing Rats

Adolescence is an age of widespread alcohol abuse, but the effect of alcohol consumption on bone formation has not been studied in the young population. This study addresses the effect of alcohol on the early phases of bone growth and development in an animal model. Four-week-old, female Sprague-Dawley rats were divided into three groups. Alcohol-treated animals were fed a modified Lieber-DeCarli diet ad libitum containing 35% ethanol-derived calories, whereas the pair-fed animals (weight-matched to ethanol rats) received an iso-caloric liquid diet in which maltose-dextrin substituted calories supplied by ethanol. Chow animals were fed a standard rat chow ad libitum. Proximal tibiae (primarily cancellous bone) and femora (primarily cortical bone) were removed for analysis after 2, 4, 6, or 8 weeks on the diets. Serum was collected for analysis of calcium levels, osteocalcin, corticosterone, growth hormone, parathyroid hormone, and 25-hydroxyvitamin D. The most rapid weight gain occurred between 6 and 8 weeks of age, and it was significantly delayed in alcohol and pair-fed animals. Almost all morphological parameters of bone were lower in the alcohol groups. No significant difference in serum calcium levels, osteocalcin, or growth hormone levels were found, and small difference in calciotropic hormone levels was found between groups. The results indicate that chronic alcohol consumption during the age of bone development reduces bone density and peak bone mass in both cortical and cancellous bone. The mechanism whereby this effect occurs is not fully understood, but, our results suggest that the negative impact of alcohol on growing bone is not due to the secondary effects of altered bone mineral regulating hormones.     

Bone Marrow Triglyceride Accumulation and Hormonal Changes During Long-Term Alcohol Intake in Male and Female Rats

BACKGROUND: Chronic alcohol consumption may influence the metabolism of adipocytes, the most abundant stromal cell phenotype in bone marrow, and promote bone marrow triglyceride accretion. METHODS: Male and female rats 35 days old were fed the Lieber-De Carli liquid diet containing 36% of the calories as alcohol and were compared with pair-fed rats given an isocaloric liquid diet in which maltose-dextrin substituted for the calories supplied by alcohol. Other control rats were fed chow ad libitum. The rats were maintained on these diets for 64 days, after which the femurs were recovered and examined. RESULTS: End weights of male and female alcohol-fed rats were significantly lower than both control groups. Femur diaphyseal bone marrow triglyceride levels were significantly increased in alcohol-fed male and female rats compared with both control groups. Femur bone marrow cavity diameters were significantly increased and cortical thickness was significantly decreased by alcohol in both males and females. Serum insulin levels were significantly decreased by alcohol only in female rats compared with the ad libitum but not the pair-fed control group, and insulin-like growth factor-1 levels were significantly reduced in male and female rats given the alcohol diet compared with both controls. Male testosterone and female estradiol levels remained unchanged. Male estradiol levels were significantly increased by alcohol compared with both controls, and female progesterone levels were significantly reduced by alcohol compared with pair-fed rats. Whereas female leptin levels were unchanged by alcohol, male leptin levels were significantly increased by alcohol compared with pair-fed rats. CONCLUSIONS: Hormonal and growth factor changes during chronic alcohol consumption accompany triglyceride accumulation in diaphyseal bone marrow and may parallel the effects of alcohol on mesenchymal stem cells and the balance between osteogenic and adipogenic lineages and their cellular progenies.     

Effect of chronic feeding of ethanol diet of “average” fat content on rat pancreas

The present study was done to determine the influence of dietary fat on the effect of ethanol on pancreatic macromolecular content and secretion. Weight-matched groups of Sprague-Dawley rats were divided into controls fed Rodent-Blox ad libitum; American Institute of Nutrition-76 (AIN-76) diet containing 12% calories as fat with 36% of carbohydrate calories replaced with 5% (weight/volume) concentration of ethanol fed ad libitum pair fed with animals given isocaloric amounts of AIN-76 diet for three to six months. Compared with Rodent-Blox fed controls, tissue content of trypsinogen, chymotrypsinogen, amylase, and lipase; specific activity and concentration of trypsinogen, chymotrypsinogen; and concentration of amylase were decreased at six months in AIN-76 fed controls. These changes did not result from diminished food intake, but were due to adaptation to the liquid diet. Animals fed AIN-76 diet plus ethanol did not show significant difference in the total content, specific activity, concentration, and secretion of digestive enzymes compared with those animals pair fed isocaloric amounts of AIN-76 diet. Activation of trypsinogen by exogenous trypsin was lower in rats fed AIN-76 diet and a similar change was observed in animals fed AIN-76 diet with ethanol for six months. These findings are in contrast to increased secretion of proteases and decreased trypsin inhibitor observed previously in animals fed ethanol in a diet containing "high" fat. These data indicate that ethanol effect on the pancreas is modified by dietary intake of fat and/or carbohydrates.     

Reversal by glucose of pancreatic amylase insufficiency in chronic alcoholic rats

Carbohydrate consumption regulates pancreatic amylase synthesis in rats. The Lieber-DeCarli 36% alcohol diet employed in chronic alcohol studies and the isocaloric control diet contain 11 and 47% of total calories from carbohydrates, respectively. Young rats fed ad libitum the 36% ethanol diet for 2 weeks obtained 1.2 g/day of carbohydrate, whereas those pair-fed with control diet received 5.8 g/day. Rats fed the 36% ethanol diet and given an intramuscular injection of a solution of 1.5 g of glucose daily for 2 weeks received twofold greater amounts of carbohydrate than saline-injected controls (2.7 versus 1.2 g). These changes in carbohydrate intake produced proportionate changes in pancreatic amylase levels. The secretory responses to cholecystokinin-octapeptide (CCK8) of acini from control and glucose-injected rats were significantly higher compared with those in the saline-injected or noninjected alcohol groups. The blood alcohol levels in glucose-injected rats were markedly reduced compared with other alcohol groups (71.7 versus 274.9 mg/dl) despite similar amounts of ethanol ingestion daily (2.4 g) in the three groups. In vitro experiments with acini from rats fed a nutritionally optimal diet revealed that high pharmacologic concentrations of ethanol, while inducing basal secretion, inhibited CCK8-stimulated amylase secretion. These results indicate that: (a) the amount of alcohol consumption does not correlate with either the levels of blood alcohol or of pancreatic amylase; (b) the carbohydrate availability in rats regulates pancreatic amylase levels despite significant levels of alcohol in blood; (c) blood alcohol levels observed in vivo may not affect synthetic and secretory processes of amylase in pancreatic acini.     

Effect of chronic alcohol consumption on tumor incidence due to dimethylnitrosamine administration

Summary To study the effect of chronic alcohol consumption on tumor development due to dimethylnitrosamine (DMN) administration, female Sprague-Dawley rats were pair-fed for 3 weeks a nutritionally adequate liquid diet containing either ethanol (36% of total calories) or isocalorically substituted carbohydrates as control diet. Thereafter, the animals were maintained on laboratory chow and tap water ad libitum for another 2 weeks and received 1.5 mg DMN i.p. per day for the first 5 days. This 5-week cycle was repeated three more times. Chronic treatment with an alcohol-containing diet was shown to significantly improve the mean survival time of DMN-treated rats compared with identically treated animals fed the control diet, but the total number of tumors observed under these experimental conditions and the target organ remained virtually unchanged.Abbreviations DMN dimethylnitrosamine - DEN diethylnitrosamine     

Alcohol Protects the Diaphragm during Dietary Restriction

We recently reported that alcoholic rat diaphragm develops greater contractile force than diaphragm of pair-fed control animals. The present experiment examines whether alcohol or dietary restriction is the more likely cause of this surprising finding. We conditioned 10 rats using a liquid diet containing ethanol as 36% of calories. Ten pair-fed control animals received an equal amount of isocaloric, ethanol-free liquid diet. Ten ad libitum control animals had unrestricted access to lab chow and water. Rats were killed after 30 weeks. Left costal diaphragm strips were studied in vitro at optimal length using direct stimulation at supramaximal voltage. Isometric force was measured and divided by muscle cross-section to compute stress. Maximal tetanic stresses developed by muscle from pair-fed controls were systematically less than alcoholic and ad libitum control values (p less than 0.0001); this did not depend on temperature (25 degrees vs. 37 degrees; p greater than 0.50). Pair-feeding increased twitch half-relaxation times (p less than 0.03) and shifted the tetanic stress-stimulation frequency relationship leftward by 10 Hz (p less than 0.01). Diaphragm of pair-fed rats continued to generate lower stresses during the fatigue caused by repeated contractions (p less than 0.01). We conclude that dietary restriction associated with pair-feeding compromises diaphragm performance in rats. Chronic alcohol consumption prevents or reverses these changes, since diaphragm function of alcoholic and ad libitum control animals was not different.     

Restricted diet rescues rat enteric motor neurones from age related cell death

BACKGROUND: Alone among autonomic neurones, enteric neurones are known to be vulnerable to age related cell death; over 50% may be lost in aging rodents. A previous study demonstrated unexpectedly that neurones of the myenteric plexus from rats fed a restricted diet appeared not to suffer from extensive cell death in contrast with previous studies of ad libitum fed animals. AIMS: To compare myenteric neurone numbers in the ileum of young and aging male Sprague-Dawley rats fed either ad libitum or a restricted diet. METHODS: Neurones were counted in whole mount preparations of rat ileum stained immunohistochemically for the pan-neuronal marker PGP9.5, for choline acetyltransferase, or for nitric oxide synthase, or with NADH or NADPH histochemistry. RESULTS: Neurone numbers in the rat myenteric plexus were substantially affected by the dietary regimen: ad libitum feeding (50-60 g per day of standard rat chow) resulted in the death of about 50% of myenteric neurones in 24 month Sprague-Dawley rats, while numbers were unchanged when the daily dietary intake was halved between the ages of six and 24 months. Animals fed a double restricted diet (15 g per day) showed no cell loss at 30 months, as well as the predicted increase in longevity. Neurone loss was largely complete by 16 months in ad libitum fed animals. Numbers of cholinergic (possibly motor) neurones, as demonstrated by choline acetyltransferase immunohistochemistry, were substantially reduced in ad libitum fed aging rats but not in animals fed a restricted diet. Loss of cholinergic neurones after ad libitum feeding was confirmed by reduced numbers of neurones of a size range matching that of cholinergic neurones. CONCLUSIONS: Ad libitum feeding of adult rats has adverse effects on the survival of myenteric neurones, neurone loss commencing before 16 months of age. Cholinergic neurones appear to be particularly vulnerable to the effects of diet. Restricting dietary intake from six months of age prevents neurone loss almost entirely up to 30 months of age in these rats.     

Modification by sex of diet and ethanol effect on rat pancreatic acinar cell metabolism

The present study was done to determine the role of sex of the animal on the effect of diet and ethanol on pancreatic acinar cell function. Weight-matched groups of Sprague-Dawley rats of either sex were divided into groups of three each and fed Wayne Lab-Blox ad libitum, Lieber-DeCarli diet with 36% of carbohydrate calories replaced with ethanol ad libitum, and Lieber-DeCarli diet in an amount isocaloric to ethanol-fed animals for a period of 3 months. Despite similar amounts of protein, fat, and carbohydrates fed to male and female rats, the female rats had lower amylase content in the tissue when fed Lieber-DeCarli diet and a higher specific activity of trypsinogen in the tissue of animals fed Lab-Blox. Specific activity of chymotrypsinogen increased in males fed Lieber-DeCarli diet and decreased in females fed the same diet when compared with animals of the same sex fed Lab-Blox. Secretion of various digestive enzymes was also different in male and female rats, whereas trypsin inhibitor secretion was similar. These data indicate different adaptive responses in male and female rats to diets with similar proportions of nutrients. When ethanol-fed male rats were compared with ethanol-fed female rats, there was a significant increase in secretion of trypsinogen and amylase (and a proportional but statistically nonsignificant increase in lipase) in female rats. These data indicate that chronic feeding of ethanol results in a nonparallel secretion of digestive enzymes in both sexes with a greater discordance between the trypsinogen secretion and trypsin inhibitor in female rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of Paternal Alcohol Consumption in Mice

Male mice were divided into four groups, one group was given ad libitum access to a liquid alcohol diet containing 35% ethanol derived calories (EDC). A second group was pair fed an isocaloric control diet containing 17.5% EDC whereas a third was similarly treated with a 0% EDC diet for a minimum of 42 days. A fourth group served as ad libitum nontreated controls to assess the role of pair feeding. Males were then mated with nontreated females. The males consuming alcohol had an increased percentage of abnormal sperm and there was a significant effect of paternal alcohol exposure on implantation sites, but no effect on pre- or postnatal mortality or fetal weight. These results suggest that paternal alcohol consumption adversely affects sperm production but does not affect development of offspring in mice.     

Aging and dietary modulation of rat skeleton and parathyroid hormone

Studies were carried out on SPF F344 male rats to evaluate the effects of aging and life-prolonging food restriction, without malnutrition, on rat skeleton and circulating PTH. Six-week-old F344 rats were divided into five groups. Group 1 rats were fed ad libitum a diet that contained 21% protein. Group 2 rats were fed 60% of the mean food intake of group 1 rats from 6 weeks of age for the rest of their lives. Group 3 rats were fed 60% of the ad libitum food intake until 6 months of age and then switched to ad libitum feeding. Group 4 rats were fed ad libitum until 6 months of age, and then switched to 60% of the ad libitum food intake. Group 5 rats were fed ad libitum a diet that contained only 12.6% protein so that these animals ingested the same amount of protein per day as the group 2 rats. In group 1 animals, bone length, weight, density, and calcium content increased rapidly with age and plateaued at about 12 months of age. There was no evidence of bone loss in these animals until about 24 months of age, but by 27 months, the animals had lost appreciable amounts of bone. The circulating immunoreactive PTH levels of the animals increased with advancing age, with a marked rise at 27 months. The age-related changes in bone and serum PTH levels of rats in groups 3 and 5 were similar to those of group 1 animals, except that a terminal increase in serum PTH did not occur in group 5 rats. In the groups 2 and 4 animals which were food restricted for the longest period, bone growth and maturation were slowed down, but the animals did not experience senile bone loss or marked terminal increase in circulating PTH. The salutary effects of food restriction were, therefore, not due specifically to the restriction of protein intake or to restricting food intake only during the period of rapid growth.     

Hormonal Changes in Rats Consuming Alcohol prior to and during Gestation

Although the fetuses of rats given alcohol prior to and during gestation are small, the placentas are large compared to those of untreated rats. It has been suggested that placental enlargement may be a consequence of a reduction in progesterone production. To investigate this, rats were given 20% ethanol in water prior to pregnancy and 30% ethanol in water throughout gestation, with rat chow ad libitum (alcohol group) or water with an equicaloric diet in which corn starch was substituted for alcohol (pair-fed group), or rat chow and water ad libitum (as libitum control group). Serum progesterone and testosterone were measured on day 17 of gestation and plasma and pituitary luteinizing hormone (LH) and follicle-stimulating hormone (FSH) on day 21 of gestation. Progesterone was significantly reduced in the alcohol but not the pair-fed group. Testosterone levels were not different among the three groups. Plasma LH was significantly reduced in both the alcohol and the pair-fed groups, but plasma FSH and pituitary LH and FSH did not differ among the three groups. These data are consistent with a possible role for progesterone in the placental enlargement seen in alcohol-fed rats.     

Pituitary and Thyroid Hormones in Pregnant Alcohol-Fed Rats and Their Fetuses

The effect of maternal alcohol consumption on serum and pituitary concentrations of hormones was investigated in pregnant rats and their fetuses. Rats were given 20% ethanol in water prior to pregnancy and 30% ethanol in water throughout gestation, with rat chow ad libitum (alcohol group), or water with an equicaloric diet in which corn starch was substituted for alcohol (pair-fed group), or rat chow and water ad libitum (ad libitum control group). Growth hormone (GH), prolactin (Prl), thyroid-stimulating hormone (TSH), thyroxine (T4), and triiodothyronine (T3) were measured in maternal serum, GH, Prl, and TSH in maternal pituitary, and GH, T4, and T3 in fetal serum. Fetuses of alcohol-fed rats weighed significantly less than fetuses of pair-fed or ad libitum controls. GH, Prl, and TSH were significantly reduced in the maternal serum of alcohol and pair-fed rats compared to ad libitum controls, but T4 and T3 did not differ among the three groups. Pituitary GH was reduced in the alcohol-fed rats, but pituitary Prl and TSH did not differ among the three groups. In the fetuses, neither GH nor T4 differed among the three groups. Fetal T3 was not detectable by this assay. It is suggested that alcohol ingestion affects maternal growth hormone levels, possibly by influencing either the synthesis or the release of the hormone from the pituitary gland. The other hormonal changes may be the result of the reduced food intake, rather than a specific effect of alcohol.     

Moderate Alcohol Consumption Does Not Augment Bone Density in Ovariectomized Rats

Moderate levels of alcohol consumption have been reported to have a beneficial effect on bone mineral density in postmenopausal women. The objective of this study was to examine the effect of a moderate level of alcohol consumption on bone density in a rigorously controlled animal model of osteoporosis. Ovariectomized and nonovariectomized rats were placed on standard lab pellets with free access to deionized water ad libitum. Alcohol-treated animals were given 0.38 g/kg of alcohol daily by intubation in the mid-afternoon and free access to standard lab pellets for 6 weeks. The amount of the alcohol solution was calculated daily to give the human equivalent of 2 glasses of wine/day. Pair-fed control animals were given, on the following day, an equal volume of the diet consumed by individual ethanol-fed rats. They received daily intubation solutions, with the ethanol replaced by isocaloric and isovolumetric amounts of maltose-dextrin. Chow-fed control animals received no intubations and were given access to standard lab pellets ad libitum. Ovariectomized animals had increased weight and decreased femur density and bone volume per total volume. They also had decreased total trabecular area, trabecular area, and number, as well as increased trabecular separation. Significant differences were found between the ovariectomized and nonovariectomized animals in the parameters under discussion, but there were no differences between diet groups. No beneficial effects were found after daily alcohol treatments.     

Effect of Exposure to an Alcohol Diet for 10 Days on the Ability of Interleukin-1β to Release ACTH and Corticosterone in the Adult Ovariectomized Female Rat

Adult ovariectomized female rats were fed an alcohol diet for 10 days. Animals fed ad libitum, or fed an isocaloric diet (pair-fed), were also included in all experiments. The intravenous injection of interleukin-β caused dose-related increases in plasma adrenocorticotropic hormone (ACTH) levels in all three groups of rats. However, alcohol-fed animals showed a significant blunting of their ACTH, but not corticosterone response, in comparison with rats fed ad libitum or pair-fed. In contrast, corticotropin-releasing factor (CRF) injection caused overall statistically comparable ACTH secretory rates in all animals, although small differences were observed in some cases. Exposure to mild electroshocks for 30 min significantly increased ACTH values in all animals, but alcohol-fed rats again showed blunted release. In this paradigm, pair-fed animals exhibited a response that was intermediate between that of the ad libitum and alcohol-fed groups.
We conclude that chronic alcohol consumption decreases the response of the hypothalamic-pituitary axis to cytokines and mild footshocks. This suggests that the activity of both CRF nerve terminals in the median eminence, and of CRF perikarya in the hypothalamus, is inhibited by this treatment, although pituitary responsiveness to CRF appears unchanged.     

Feeding Patterns of Rats Chronically Ingesting an Ethanol-Containing Liquid Diet

We compared the feeding patterns of rats ingesting a 36% ethanol-containing liquid diet for 30 days with those of rats pair-fed an isocaloric liquid control diet or provided control diet or ground rat chow ad libitum. Ethanol-fed rats consumed fewer calories per day and gained less body weight than rats fed control diets ad libitum. Daily caloric intakes were ∼50% lower during the first 10 days and 20% thereafter. Lower intakes in ethanol-fed rats occurred through a decrease in mean meal size rather than number of meals per day, although meals were more evenly distributed diurnally. Pair-fed rats ingested most of their food in one or two meals within a few hours of presentation. In a related experiment, a 4-hr duodenal infusion of ethanol at a rate comparable to that of ethanol ingestion resulted in plasma ethanol levels of 28 ± 4 mM and suppressed 5-hr intake by ∼40% by increasing the mean postmeal interval and satiety ratio. These results suggest that the suppressive effect of ethanol ingestion on food intake may be mediated in part by a post-gastric mechanism of ethanol action.     

Long-term alcohol consumption in the rat affects femur cross-sectional geometry and bone tissue material properties

BACKGROUND: Alcohol consumption previously has been demonstrated to reduce the density and strength of cortical bone of young, actively growing rats. Osteoblast activity and trabecular bone volume were also significantly lower. A germane question arising from these studies is whether the detrimental effects would persist into adulthood. To address this issue, a long-term study was undertaken with animals that consumed alcohol throughout their life and into old age. METHODS: One-month-old female Sprague-Dawley rats were divided into three diet groups: alcohol-fed, pair-fed, and chow-fed. The alcohol-fed animals received a modified Lieber-DeCarli diet that contained 35% ethanol-derived calories. The pair-fed group served as a caloric-equivalent control, and the chow-fed animals served as a completely untreated control. Animals were euthanized after five time periods on the diets that represented three stages of the life span: young (3 months), adult (6, 9, 12 months), and aged (18 months). The left femur was isolated and mechanically tested in 3-point bending for mechanical properties. RESULTS: In the young animals, alcohol consumption produced dramatic reductions in both extrinsic (whole bone) and intrinsic (tissue material) properties, which is consistent with results from previous studies on growing rats. For the adult animals, however, the alcohol groups were only slightly lower and the differences were not statistically significant. The aged animals showed diminished properties due to alcohol, but only for the intrinsic material properties. The extrinsic properties remained similar to controls as a result of greater radial expansion in the femur diaphysis. Despite the cross-sectional areas being the same, this expansion gave rise to higher cross-sectional moment of inertia values in the alcohol animals. The thickness of the cortical wall was lowest in the alcohol group at all time points. CONCLUSIONS: Long-term alcohol consumption produced two major effects in the oldest animals studied: the quality of the cortical bone tissue was diminished, as evidenced by reduced elastic modulus and ultimate strength values, and the bone seemed to compensate for this by expanding the cross-section to produce larger cross-sectional moment of inertia values. The reduced bone tissue quality is consistent with the lower ash percent values in the alcohol animals, but other factors such as the quality of the collagen and mineral crystal may also be important contributors.     

Effect of prolonged ethanol intake on pancreatic lipids in the rat pancreas

Although fat accumulation in acinar cells is the earliest histopathological change in the pancreas of patients and experimental animals, there are few long-term studies regarding lipid composition of the pancreas in alcoholism. In the present study, female Sprague-Dawley rats were divided into three groups each fed Wayne Rodent-Blox ad libitum or Lieber-DeCarli diet with 36% of maltose dextrin calories replaced with ethanol ad libitum, or isocaloric amounts of liquid diet for a period of 21 months resulting in changes of chronic pancreatitis in ethanol-fed rats. A low level of triglycerides, a high level of cholesterol ester and moderately elevated phospholipids, low incorporation of [14C]palmitoyl in triglycerides, increased 14C activity in phospholipids, and cholesterol ester were found by thin-layer chromatography in ethanol-fed rats. These data indicate that the pancreas synthesized triglycerides and other lipid components in the same way as liver and fat cells. Chronic ethanol ingestion caused marked changes in pancreatic lipid metabolism due to altered enzyme activities involved in the lipid pathways.