Body size and pubertal development explain ethnic differences in structural geometry at the femur in Asian, Hispanic, and white early adolescent girls living in the U.S.

UNLABELLED: Variation in structural geometry is present in adulthood, but when this variation arises and what influences this variation prior to adulthood remains poorly understood. Ethnicity is commonly the focus of research of skeletal integrity and appears to explain some of the variation in quantification of bone tissue. However, why ethnicity explains variation in skeletal integrity is unclear. METHODS: Here we examine predictors of bone cross sectional area (CSA) and section modulus (Z), measured using dual-energy X-ray absorptiometry (DXA) and the Advanced Hip Analysis (AHA) program at the narrow neck of the femur in adolescent (9-14 years) girls (n=479) living in the United States who were classified as Asian, Hispanic, or white if the subject was 75% of a given group based on parental reported ethnicity. Protocols for measuring height and weight follow standardized procedures. Total body lean mass (LM) and total body fat mass (FM) were quantified in kilograms using DXA. Total dietary and total dairy calcium intakes from the previous month were estimated by the use of an electronic semi-quantitative food frequency questionnaire (eFFQ). Physical activity was estimated for the previous year by a validated self-administered modifiable activity questionnaire for adolescents with energy expenditure calculated from the metabolic equivalent (MET) values from the Compendium of Physical Activities. Multiple regression models were developed to predict CSA and Z. RESULTS: Age, time from menarche, total body lean mass (LM), total body fat mass (FM), height, total calcium, and total dairy calcium all shared a significant (p<0.05), positive relationship with CSA. Age, time from menarche, LM, FM, and height shared significant (p<0.05), positive relationships with Z. For both CSA and Z, LM was the most important covariate. Physical activity was not a significant predictor of geometry at the femoral neck (p≥0.339), even after removing LM as a covariate. After adjusting for covariates, ethnicity was not a significant predictor in regression models for CSA and Z. CONCLUSION: Variability in bone geometry at the narrow neck of the femur is best explained by body size and pubertal maturation. After controlling for these covariates there were no differences in bone geometry between ethnic groups.

Bone mineral and predictors of bone mass in white, Hispanic, and Asian early pubertal girls.

Differences in bone among racial/ethnic groups may be explained by differences in body size and shape. Previous studies have not completely explained differences among white, Asian, and Hispanic groups during growth. To determine racial/ethnic differences and predictors of bone mass in early pubertal girls, we measured bone mineral content (BMC) in white, Hispanic, and Asian sixth-grade girls across six states in the United States. We developed models for predicting BMC for the total-body, distal radius, total-hip, and lumbar spine for 748 subjects. For each of the bone sites, the corresponding area from dual-energy X-ray absorptiometry (DXA) was a strong predictor of BMC, with correlations ranging 0.78-0.98, confirming that larger subjects have more BMC. Anthropometric measures of bone area were nearly as effective as bone area from DXA at predicting BMC. For total-body, distal radius, lumbar spine, and total-hip BMC, racial/ethnic differences were explained by differences in bone area, sexual maturity, physical activity, and dairy calcium intake. Bone size explained most of the racial/ethnic differences in BMC, although behavioral indicators were also significant predictors of BMC.

Lactose maldigestion, calcium intake and osteoporosis in African-, Asian-, and Hispanic-Americans.

Dietary calcium is critical for the development of the human skeleton and likely plays an important role in the prevention of osteoporosis. Dairy products provide approximately three-fourths of calcium consumed in the diet and are the most concentrated sources of this essential nutrient. One obstacle that likely interferes with calcium consumption among many ethnic groups is lactose maldigestion. The real or perceived occurrence of intolerance symptoms after dairy food consumption may cause maldigesters to avoid dairy products. Several investigators have observed a relationship between lactose maldigestion, dietary calcium and osteoporosis in Caucasian populations. Research on ethnically diverse populations is necessary to better understand how lactose maldigestion influences the risk for osteoporosis. Low calcium intakes, a greater than previously thought potential for low bone density and extensive lactose maldigestion among Hispanic-American and Asian-American populations may create an elevated risk for osteoporosis. Dietary management strategies for lactose maldigesters to increase calcium consumption include consuming (1) dairy foods with meals, (2) yogurts, (3) calcium-fortified foods, (4) using lactose digestive aids and (5) including dairy foods daily in the diet to enhance colonic metabolism of lactose.

Dietary fiber and colorectal cancer: what is appropriate advice?

Two recent studies question the role of dietary fiber in the prevention of colorectal cancer. However, the duration of dietary intervention, dose of fiber, and the complexity of polyp formation and transformation to carcinomas make interpretation of such studies difficult. Multiple rationales exist for promoting the consumption of high-fiber, low-fat, fruit- and vegetable-rich diets.

Improved lactose digestion and intolerance among African-American adolescent girls fed a dairy-rich diet.

OBJECTIVE: To determine whether African-American adolescent girls who were fed a dairy-rich diet for 21 days could adapt to lactose, experiencing an overall improvement in lactose tolerance as well as a decrease in hydrogen gas production. DESIGN: Twenty-one-day dietary intervention study. SUBJECTS/SETTING: Seventeen of 21 African-American girls (aged 11 to 15 years) enrolled in a calcium metabolism study chose to participate in the lactose tolerance study. Subjects were screened for any diseases, conditions, or medications that might alter calcium metabolism or colonic fermentation. Subjects were housed in a fraternity on the Purdue University, West Lafayette, Ind, campus, and were supervised 24 hours a day. INTERVENTION: Subjects consumed a dairy-based diet averaging 1,200 mg calcium and 33 g lactose per day for 21 days. Lactose digestion was assessed by an 8-hour breath hydrogen test on days 1 and 21, and symptoms of intolerance (abdominal pain, bloating, flatulence, and diarrhea) were evaluated hourly on a ranked scale during the breath hydrogen tests and once each evening during the 21-day feeding period. MAIN OUTCOME MEASURES: A comparison of breath hydrogen production and gastrointestinal symptoms at the beginning and end of the study. STATISTICAL ANALYSES PERFORMED: The Wilcoxon signed ranks test was used to compare the area under the curve for the 2 breath hydrogen tests. Spearman's p test for trend was used to determine whether there was a change in symptoms. All statistical analyses were 2-tailed and significance was set at P = .05. RESULTS: Fourteen of the 17 subjects had lactose maldigestion. Breath hydrogen excretion decreased significantly (P < .03) from the beginning (148.3 +/- 27.0 ppm x hours) to the end (100.7 +/- 19.3 ppm x hours) of the 21-day period. Gastrointestinal symptoms were negligible during both the breath hydrogen tests as were symptoms during the 21-day period. APPLICATIONS/CONCLUSIONS: The diet was well tolerated by the subjects. Furthermore, the decrease in breath hydrogen suggests colonic adaptation to the high-lactose diet. The results indicate that lactose maldigestion should not be a restricting factor in developing adequate calcium diets for this population. The existence of lactose maldigestion does not result in lactose intolerance in this population when it is fed a dairy-rich diet.

Cardiovascular disease and fiber: is insulin resistance the missing link?

Multiple mechanisms are likely for any effect of fiber on cardiovascular disease risk. One component that is described is the hypocholesterolemic activity of soluble fibers as they bind bile acids. New epidemiologic evidence indicates that fiber's modulation of insulin secretion and resistance deserves additional attention.

Modification of colonic fermentation by bifidobacteria and pH in vitro. Impact on lactose metabolism, short-chain fatty acid, and lactate production.

Colonic fermentation plays an important role in the prevention of lactose intolerance and intestinal disorders. The objectives of this study were to evaluate whether supplementation with bifidobacteria modify colonic fermentation of lactose and short-chain fatty acid production and to assess influence of the pH in an in vitro continuous culture system. There was a significantly greater reduction in lactose concentrations at pH 6.7 than that at either pH 6.2 or pH 5.7, accompanied by the highest beta-galactosidase activity and D-lactate production. Bifidus supplementation reduced lactose and D-lactate concentrations and increased acetate production at pH 6.7. The study demonstrates that lactose is rapidly metabolized by colonic bacteria and lactose fermentation in vitro is pH dependent with a maximum rate at pH 6.7. Bifidobacteria supplementation may have the potential to improve lactose fermentation and to manipulate SCFA and lactate production.

In vitro lactose fermentation by human colonic bacteria is modified by Lactobacillus acidophilus supplementation.

Adaptation of the colonic flora to lactose may contribute to lactose digestion in lactose maldigesters, and supplementation with Lactobacillus acidophilus may modify colonic fermentation of lactose and short-chain fatty acid production. We evaluated the capability of colonic bacteria to ferment lactose and the ability of L. acidophilus to modify lactose fermentation by the colonic microflora in vitro. An anaerobic continuous culture was established and inoculated with fresh samples of human feces. Lactose infusion was maintained at 25 g/d and pH at 6.7. L. acidophilus strain LA-1 (1.5 x 10(10) cells) was introduced into the fermenter on d 0 or added daily on d 0 through 4. The control was the continuous culture without the addition of lactobacilli. Rapid adaptation of colonic bacteria to lactose occurred within 1-2 d, with a significant decrease in lactose concentration and increase in beta-galactosidase activity, and lactose concentrations fell below 3 mmol/L by d 7. Supplementation with strain LA-1 resulted in a significantly greater decrease in lactose concentration and greater increase in acetate and propionate production within the first day compared with the control group. However, there was no significant difference between the fermentation treated with L. acidophilus daily and the control after the first day. These data suggest that the colonic bacteria adapt quickly to lactose, causing efficient utilization of lactose. L. acidophilus supplementation may enhance lactose fermentation during early periods when the adaptation is not established in this model.

Improvement of lactose digestion by humans following ingestion of unfermented acidophilus milk: influence of bile sensitivity, lactose transport, and acid tolerance of Lactobacillus acidophilus.

The influence of bile sensitivity, lactose transport, and acid tolerance of Lactobacillus acidophilus on in vivo digestion of lactose was investigated. Four strains of L. acidophilus exhibiting varied degrees of lactose transport, beta-galactosidase activity, and bile sensitivity were used to prepare unfermented acidophilus milks. Lactose malabsorption was evaluated by measuring breath H2 excretion off 11 lactose maldigesting subjects following ingestion of four acidophilus test milks. Test meals were fed in a randomized double-blind protocol. Consumption of acidophilus milk (2% fat) containing strains B, N1, and E significantly reduced mean total H2 production compared with that of the control reduced-fat (2% fat) milk, but milk containing strain ATCC 4356 did not differ from the control. Acidophilus milk containing L. acidophilus N1 was the most effective of the four acidophilus milks in improving lactose digestion and tolerance. Strain N1 exhibited the lowest beta-galactosidase activity and lactose transport but the greatest bile and acid tolerance of the four strains. The results indicated that bile and acid tolerance may be important factors to consider when L. acidophilus strains are selected for improving lactose digestion and tolerance.

Fecal hydrogen production and consumption measurements. Response to daily lactose ingestion by lactose maldigesters.

The alteration of hydrogen (H2) metabolism, which accounts for the large decrease in breath H2 excretion following prolonged ingestion of malabsorbed carbohydrate (lactulose, lactose in lactose maldigesters) was studied in six lactose-maldigesting adults. Metabolic inhibitors of the three main H2-consuming reactions (methanogenesis, sulfate reduction, and acetogenesis) were used to independently measure H2 production and consumption in fecal samples obtained after 10 days of either dextrose or lactose feeding. Absolute fecal H2 production (net of production minus consumption) after 3 hr of incubation with lactose was approximately threefold lower after lactose adaptation (242 +/- 54 microliters) compared to dextrose adaptation (680 +/- 79 microliters, P = 0.006). Fecal H2 consumption was not affected by either feeding period. We conclude that decreased absolute H2 production, rather than increased H2 consumption, is responsible for the decrease in breath H2 observed with lactose feeding.

Colonic adaptation to daily lactose feeding in lactose maldigesters reduces lactose intolerance.

We conducted blinded, controlled crossover studies to determine the effect of daily lactose feeding on colonic adaptation and intolerance symptoms. The initial study with nine lactose maldigesters showed a threefold increase in fecal beta-galactosidase activity after 16 d of lactose feeding. To determine the effects of this adaptation on breath hydrogen and intolerance symptoms, 20 lactose-maldigesting adults were randomly assigned to lactose or dextrose supplementation for 10 d (days 1-10), crossing over to the other period for days 12-21. The sugar dosage was increased from 0.6 to 1.0 g.kg-1.d-1, subdivided into three equal doses, by adjusting the dose every other day. Symptoms during lactose supplementation and comparison of symptoms during the lactose and dextrose feeding periods showed no significant differences. On days 11 and 22, challenge doses of lactose (0.35 g/kg) were administered after an overnight fast, and breath hydrogen and intolerance symptoms (abdominal pain, flatulence, and diarrhea) were carefully monitored for 8 h. Frequency of flatus passage and flatus severity ratings after the lactose challenge decreased 50% when studied at the end of the lactose period compared with the dextrose period. The sum of hourly breath-hydrogen concentrations (1-8 h) was significantly reduced after the lactose feeding period (9 +/- 38 ppm.h) compared with after the dextrose period (385 +/- 52 ppm.h, P < 0.001). We conclude that there is colonic adaptation to regular lactose ingestion and this adaptation reduces lactose intolerance symptoms.

Improvement of lactose digestion in humans by ingestion of unfermented milk containing Bifidobacterium longum.

Fifteen lactose malabsorbers were studied to evaluate the effects of consumption of milk containing different strains of Bifidobacterium longum on lactose digestion. Influences of different growth substrates, bile sensitivity, and lactose transport on lactose digestion by bifidobacteria were also investigated. Lactose malabsorption was determined by measuring breath hydrogen excretion of subjects fed four different test milks (three of which contained 5 x 10(8) cfu/ml of B. longum) on 4 different d using a randomized, double-blinded trial. Test milks included 1) 400 ml of lowfat milk (control), 2) 400 ml of milk containing B. longum B6 that had been grown with lactose, 3) 400 ml of milk containing B. longum B6 grown with lactose plus glucose, or 4) 400 ml of milk containing B. longum ATCC 15708 grown with lactose. beta-Galactosidase activity was highest in milk containing B6 grown with lactose but was extremely low in milk containing B6 grown with lactose and glucose. Consumption of milk containing B6 grown with lactose resulted in significantly less hydrogen production and flatulence than occurring after consumption of control milk or the milk containing B6 grown with both lactose and glucose. Hydrogen production after ingestion of 15708 was also significantly lower than hydrogen production after ingestion of the control milk. We concluded that milks containing B. longum might reduce breath hydrogen response and symptoms from lactose malabsorption when the culture is grown in a medium containing only lactose to induce a higher beta-galactosidase level and increase rate of lactose uptake.

How much lactose is low lactose?

OBJECTIVE: To test the hypothesis that complete elimination of lactose is not necessary to ensure tolerance by lactose maldigesters. DESIGN: Double-blind, randomized protocol in which challenge doses of 0, 2, 6, 12, and 20 g lactose in water were fed to subjects after a 12-hour fast. SUBJECTS: 13 healthy, free-living adults who were lactose maldigesters. MAIN OUTCOME MEASURES: Breath hydrogen production (a measure of maldigestion) and symptom response to each challenge dose. STATISTICAL ANALYSIS: Analysis of variance was done to determine overall differences in mean hydrogen gas production (peak and sum of hours 1 through 8). Friedman's test was used to determine overall differences in the mean ranks for each symptom. Fisher's least significant difference test was used for multiple comparisons for hydrogen and symptom and data. RESULTS: Hydrogen production after consumption of the 0- and 2-g lactose doses was not significantly different. Hydrogen production increased with the 6-g dose. Intensity of abdominal pain increased when the dose of lactose was 12 g. Episodes of flatulence did not increase until the dose reached 20 g. No significant differences in the occurrence of diarrhea were observed after the five treatments. CONCLUSIONS: No significant increase in breath hydrogen production or intolerance symptoms occurred after consumption of a 2-g dose of lactose. Up to 6 g was tolerated, even though maldigestion could be measured at the 6-g dose. Thus, lactose maldigesters may be able to tolerate foods containing 6 g lactose or less per serving, such as hard cheeses and small servings (120 mL or less) of milk.

Review article: the treatment of lactose intolerance.

While about 50 million Americans malabsorb lactose, the colonic metabolism of this disaccharide may prevent the symptomatic state known as lactose intolerance. Elucidation of the clinical importance of lactose malabsorption requires comparison of symptoms after ingestion of lactose with those following an identical appearing lactose-free control. This paper reviews the extensive literature concerning lactose-induced symptoms and the value of lactose digestive aids. Poorly controlled studies have suggested that a cup of milk results in appreciable symptoms in the majority of lactase-deficient subjects. In contrast, controlled trials in unselected lactose malabsorbers of subjects claiming severe lactose intolerance indicate that symptoms from a cup of milk are no greater than that with a lactose-hydrolyzed control. An increasing fraction of subjects experience symptoms as the lactose load is increased, with the majority having symptoms when the equivalent of 1 L of milk is ingested as a single dose. Further studies are required to determine the tolerance to several cups of milk taken throughout the day. Available digestive aids include pre-hydrolyzed milk and lactase preparations that can be added to milk (which is then incubated) or ingested with milk. While these products are effective in reducing symptoms, it should be emphasized that there appears to be no need for these preparations when the dosage of milk is limited to one cup per day.

A comparison of symptoms after the consumption of milk or lactose-hydrolyzed milk by people with self-reported severe lactose intolerance.

BACKGROUND: Ingestion of a large dose of the milk sugar lactose--for example, the 50-g load in 1 liter of milk--causes symptoms such as abdominal pain, diarrhea, bloating, and flatulence in the majority of people with lactose malabsorption. It is uncertain whether the ingestion of more common doses of lactose, such as the amount in 240 ml (8 oz) of milk, causes symptoms. Some people insist that even smaller quantities of milk, such as the amount used with cereal or coffee, cause severe gastrointestinal distress. METHODS: In a randomized, double-blind, crossover trial, we evaluated gastrointestinal symptoms in 30 people (mean age, 29.4 years; range, 18 to 50) who reported severe lactose intolerance and said they consistently had symptoms after ingesting less than 240 ml of milk. The ability to digest lactose was assessed by measuring the subjects' end-alveolar hydrogen concentration after they ingested 15 g of lactose in 250 ml of water. Subjects then received either 240 ml of lactose-hydrolyzed milk containing 2 percent fat or 240 ml of milk containing 2 percent fat and sweetened with aspartame to approximate the taste of lactose-hydrolyzed milk; each type of milk was administered daily with breakfast for a one-week period. Using a standardized scale, subjects rated the occurrence and severity of bloating, abdominal pain, diarrhea, and flatus and recorded each passage of flatus. RESULTS: Twenty-one participants were classified as having lactose malabsorption and nine as being able to absorb lactose. During the study periods, gastrointestinal symptoms were minimal (mean symptom-severity scores for bloating, abdominal pain, diarrhea, and flatus between 0.1 and 1.2 [1 indicated trivial symptoms; and 2, mild symptoms]). When the periods were compared, there were no statistically significant differences in the severity of these four gastrointestinal symptoms. For the lactose-malabsorption group, the mean (+/- SEM) difference in episodes of flatus per day was 2.5 +/- 1.1 (95 percent confidence interval, 0.2 to 4.8). Daily dietary records indicated a high degree of compliance, with no additional sources of lactose reported. CONCLUSIONS: People who identify themselves as severely lactose-intolerant may mistakenly attribute a variety of abdominal symptoms to lactose intolerance. When lactose intake is limited to the equivalent of 240 ml of milk or less a day, symptoms are likely to be negligible and the use of lactose-digestive aids unnecessary.

Factors affecting the ability of a high beta-galactosidase yogurt to enhance lactose absorption.

Lactose in yogurt is better absorbed by lactase-deficient subjects than is an equivalent quantity of lactose in milk, presumably because of the microbial activity of the beta-galactosidase present in yogurt. In this study, we describe a process that increases the beta-galactosidase of yogurt 5- to 6-fold and the ability of this high lactase yogurt to enhance lactose absorption in lactase-deficient subjects. These subjects ingested the yogurt meals after a 12-h fast, and lactose malabsorption was determined by measuring breath hydrogen. Breath hydrogen was reduced 39% following ingestion of high lactase yogurt from that after consumption of conventional yogurt, indicating that the high lactase yogurt enhanced lactose absorption. However, the reduction after high lactase yogurt was less than expected, given the 5- to 6-fold increment in beta-galactosidase measured in vitro. In vivo activity of beta-galactosidase requires that the enzyme resist acid denaturation in the stomach. The beta-galactosidase in high lactase yogurt was much less acid resistant than was the beta-galactosidase in conventional yogurt, and the relative inability of high lactase yogurt to enhance lactose absorption was likely due to the destruction of the beta-galactosidase in the stomach.

Lactose digestion and tolerance in adult and elderly Asian-Americans.

Twenty adult (20-40-y old) and 20 elderly (> or = 65-y old) Asian-Americans subjects were evaluated for baseline lactose consumption, fecal beta-galactosidase activity, and lactose maldigestion to determine whether there were differences in lactose metabolism and tolerance between these groups. Fasted subjects consumed a challenge dose of 0.5 g lactose/kg body wt. Breath-hydrogen production and symptoms were monitored. There were no statistically significant differences in total hydrogen production (P < 0.6), flatulence (P < 0.6), or fecal beta-galactosidase activity between the two groups. Fecal beta-galactosidase activity did not correlate with prior lactose consumption. The shape of the breath-hydrogen curves suggests a slightly delayed transit in the elderly subjects, but apparently this delay was insufficient to alter tolerance. Thus, the findings suggest that these two groups do not differ in their metabolism and tolerance of lactose.

Comparative effects of exogenous lactase (beta-galactosidase) preparations on in vivo lactose digestion.

Microbial-derived beta-galactosidase (beta-gal) enzyme preparations improve in vivo lactose digestion and tolerance through enhanced gastrointestinal digestion of lactose. Three different beta-gal preparations, Lactogest (soft gel capsule), Lactaid (caplet), and DairyEase (chewable tablet) and placebo were fed to lactose maldigesters with either 20 g or 50 g of lactose to compare the efficacy of these products and to further establish a dose-response relationship for use. All enzyme preparations dramatically reduced both the peak and total breath hydrogen production when fed with milk containing 20 g of lactose. Four capsules of Lactogest, two caplets of Lactaid, or two tablets of DairyEase (each treatment containing approx 6000 IU) reduced total hydrogen production significantly (P < 0.05) below that observed with two capsules of Lactogest (containing approx 3000 IU) in a stoichiometric manner. Symptoms were significantly (P < 0.05) less severe with all the beta-gal products. In contrast, with 50 g of lactose in water, peak and total hydrogen production was modestly, but not significantly reduced by the enzyme treatment. Furthermore, symptom scores for bloating, cramping, nausea, pain, diarrhea, and flatus were not different between treatments and the control. The 50-g lactose dose appeared to overwhelm the ability of either 3000 or 6000 IU of beta-gal to assist significantly with lactose digestion. Results from these studies demonstrate the relative equivalency of chewable, caplet, and soft-gel beta-gal products, based on IUs of enzyme fed.

Effect of development and nutritional state on the uptake, metabolism and release of free and acetyl-L-carnitine by the rodent small intestine.

Intestinal carnitine levels and the incorporation and release of exogenous, [14C]carnitine were compared in intestine from adult rat and guinea pig. Total carnitine levels were 4-fold higher in rat as compared to guinea pig intestine. Retention of label was also 4-fold greater, 4 h after placing carnitine (7 nmol) in the lumen. Carnitine was detected in rat chow (64 nmol/g) but not in guinea pig chow. Intestinal carnitine was reduced 2-fold in rats fed a carnitine-free diet for 2 weeks, suggesting the importance of dietary carnitine in determining intestinal carnitine levels. Two conditions where fatty acid oxidation is increased (fasting and suckling) resulted in elevated carnitine levels and retention. In the 3-day fasted guinea pig, intestinal carnitine increased by 40% and retention of a lumenal dose of [14C]carnitine increased about 7-fold after 4 h. During suckling, carnitine levels peaked after 3 days (792 nmol/g) and decreased to near adult levels after 7 days (108 nmol/g). Retention of a lumenal dose of carnitine was greater after 4 h in 1-day old neonatal, than in adult intestine (82% vs. 7% of a 7 nmol dose, respectively). This reflects, in part, the larger intestinal carnitine pool on day 1 (352 nmol/g) than on day 29 (91 nmol/g). The calculated efflux of total intestinal carnitine after 4 h was similar for adults and neonates (72 vs. 58 nmol/g) suggesting that efflux relative to pool size was greater in the adult than in the neonate. Uptake of [14C]acetylcarnitine was similar to [14C]carnitine in 1-day old animals, but was retained to a lesser extent (36% vs. 82%, respectively) after 4 h. The calculated efflux of total intestinal carnitine when acetylcarnitine was the substrate was about 4-fold that when carnitine was the substrate. Incorporation of [14C]carnitine into enterocytes isolated from 3-day old animals was 4-fold greater than into enterocytes isolated from adults (152 vs. 36 pmol/mg protein after 60 min). Active transport of carnitine into enterocytes from neonates, but not from adults is suggested, since labeled free intracellular carnitine reached 4-fold the calculated equilibrium value in neonatal enterocytes, but did not exceed the equilibrium value in adult enterocytes.

The neonatal guinea pig as a model for human galactose metabolism: galactose-1-phosphate uridyltransferase activity.

The specific activity of galactose-1-phosphate uridyltransferase was measured in fetal and neonatal guinea pig liver during the first 10 days of age. Activity was approximately six times greater than in adult animals, and peaked during the first 48 h after birth. Activity dropped sharply during the next 2 days, followed by a gradual decline. Liver galactose and glycogen levels were stable throughout the study period. Liver glucose rose significantly after birth, then dropped slightly. The pattern of uridyltransferase in the guinea pig is similar to that reported for phosphoenolpyruvate carboxylkinase and pyruvate carboxylase. Compared to the rat, specific activity of uridyltransferase peaked earlier, possibly due to the guinea pig's advanced maturity.