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The Journal of Nutrition Vol. 127 No. 1 January 1997, pp. 171-176
Copyright ©1997 by the American Society for Nutritional Sciences

Sodium Mercaptoacetate Is Not a Useful Probe to Study the Role of Fat in Regulation of Feed Intake in Dairy Cattle1,2

Byung-Ryul Choi*, Donald L. Palmquist*, 3, and Michael S. Allendagger

* Department of Animal Sciences, Ohio Agricultural Research and Development Center, The Ohio State University, Wooster, OH 44691-4096 and dagger  Department of Animal Science, Michigan State University, East Lansing, MI 48824

ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
FOOTNOTES
ACKNOWLEDGMENTS
LITERATURE CITED

ABSTRACT

Inhibition of fatty acid oxidation by mercaptoacetate stimulates food intake of rats fed dietary fat. To study regulation of feed intake of ruminants fed fat, dry matter intake and plasma concentrations of insulin and metabolites were determined in eight nonpregnant Holstein heifers in a cross-over design with two 14-d feeding periods by using a 2 × 2 factorial arrangement of treatments. Treatments were combinations of diet (27 or 103 g fatty acids/kg food dry matter) and injection (mercaptoacetate or saline). Half the heifers were fed each diet in Period 1, and diets were reversed in Period 2. On d 10 of each period, two animals per treatment were injected intravenously with either mercaptoacetate (300 µmol/kg body weight0.75) or saline at 2 h postfeeding. Injections were reversed on d 12. Dry matter intake was suppressed by the high fat diet. Intravenous injection of mercaptoacetate decreased dry matter intake to 25% that of the control during 4 h postinjection. Both the high fat diet and mercaptoacetate injection increased plasma non-esterified fatty acid concentration, whereas plasma beta -hydroxybutyrate concentration was lowered by the high fat diet and by mercaptoacetate injection. Plasma triglyceride concentration was increased by the high fat diet, but was decreased by mercaptoacetate injection. Mercaptoacetate elevated plasma glucose concentrations at 2 and 3 h postinjection, possibly because plasma insulin concentration was lower. Effects of mercaptoacetate on plasma insulin and metabolite concentrations may have been confounded by the effects of decreased feed intake. Therefore, direct effects of mercaptoacetate injection were not separated from effects of feed intake on plasma insulin and metabolite concentrations. Because mercaptoacetate injection decreased dry matter intake it was not a useful probe to study mechanisms of feed intake regulation in dairy cattle fed fat.

Key words: ruminant, feed intake, dietary fat, fatty acid oxidation, mercaptoacetate.

INTRODUCTION

Dietary fat increases the energy density of a diet and may increase energy intake by dairy cattle. However, feeding high fat diets often results in decreased feed and energy intakes in dairy cattle. Mechanisms that mediate fat-induced depression of feed intake have not been fully investigated in ruminants. Fat consumed by dairy cattle in excess of metabolic capacity may generate satiety signals to prevent overconsumption (Palmquist 1994). Circulating lipid metabolites may serve as signals to the satiety center in the central nervous system. Feeding fat usually increases plasma non-esterified fatty acid (NEFA)4 concentrations (Choi and Palmquist 1995), which increases hepatic uptake and oxidation of NEFA in ruminants (Pethick et al. 1984). Reducing equivalents generated from fatty acid oxidation may be involved in the control of feeding behavior in ruminants (Emery et al. 1992). The rate of energy production from fatty acid oxidation is sensed by the central satiety center through signals generated by hepatic chemoreceptive vagal afferent nerves (Langhans and Scharrer 1987). Inhibition of fatty acid oxidation by fat antimetabolites stimulated food intake in rats fed diets rich in fat (Friedman et al. 1986, Scharrer and Langhans 1986, Singer and Ritter 1994). In a recent study of lactating cows, high fat diets did not increase plasma beta -hydroxybutyrate (BHBA) concentration, an indicator of fatty acid oxidation, whereas plasma NEFA concentrations were increased by feeding fat (Choi and Palmquist, 1995). Direct evidence concerning the role of fatty acid oxidation in regulation of feed intake when high fat diets are consumed remains to be gained. The objective of this study was to test the hypothesis that inhibition of fatty acid oxidation by sodium mercaptoacetate reverses depression of feed intake in dairy cattle fed a high fat diet.

MATERIALS AND METHODS

Experimental design, diets, and animal management. Eight growing Holstein heifers averaging 397 ± 19 kg body weight from the dairy herd at Michigan State University were used in a cross-over design using a 2 × 2 factorial arrangement of treatments with two 14-d feeding periods. Treatments were diets (low vs. high fat) and injections (MA vs. saline). Diets as total mixed rations consisted of corn silage, cracked corn, soybean meal, and a vitamin and mineral mixture. In the high fat diet, Energy Booster 100® (Milk Specialties, Dundee, IL), a ruminally-inert fat, replaced an isoenergetic amount of cracked corn in the total mixed rations. Total fatty acid concentrations were 27 and 103 g/kg diet dry matter for the low and high fat diets, respectively. All diets were formulated to contain 140 g crude protein/kg diet dry matter, using soybean meal for adjustments. Ingredients and nutrient composition are listed in Table 1. Individual heifers were housed in a tie stall barn throughout the experiment and fed once daily at 0820 h. Half the animals were fed each diet in Period 1, and diets were reversed in Period 2. Animals were allowed to drink water ad libitum. The experimental protocol was reviewed and approved by the Michigan State University Animal Care and Use Committee.

Table 1. Feed ingredients and nutrient composition of diets

[View Table]

Preparation of sodium mercaptoacetate, catheterization, and injections. Sodium mercaptoacetate (Sigma, St. Louis, MO) was dissolved in saline solution (8.7 g NaCl/L) at a concentraiton of 0.15 mol/L and stored at 4°C until injection.

Polyethylene tubing (I.D. 1.19 mm, O.D. 1.70 mm, Intramedic® non-radiopaque polyethylene tubing, Becton Dickinson, Parsipanny, NJ) was inserted unilaterally into the jugular vein by aseptic procedures 2 d before initiation of injections. Catheter patency was maintained by flushing with heparinized saline solution (100,000 USP units of heparin/L) between sampling days and with sodium citrate solution (77.5 mmol/L) between blood samples.

Except for sampling days, heifers consumed feed ad libitum. At 2 h after feeding on d 10 and d 12 of each period, either mercaptoacetate (MA) (300 µmol/kg body weight0.75; 45 mL/100 kg body weight) or the same volume of saline was injected through the jugular catheter into two animals per treatment. Injections were reversed on d 12. The dose was determined in a preliminary study in which any side effects of intravenous MA injection were tested in dairy cattle; dosages >300 µmol/kg body weight0.75 caused mild fever.

Feed intake measurement. Feed disappearance was measured continuously up to 24 h after feeding on each injection day with monitors and a computerized data acquisition system described by Dado and Allen (1993). Quantity of dry matter consumed after injection, recorded at 2, 4, 10, and 22 h, was used for analysis of treatment effects.

Each feed ingredient and orts were collected daily during the injection trial in proportion to the amounts offered and refused, and composited by animal and treatment. Dry matter contents were determined at 100°C using a forced-air oven. Composited feed samples were lyophilized, ground in a Wiley mill through a 1-mm screen (Arthur H. Thomas, Philadelphia, PA), and analyzed for neutral detergent fiber (Procedure A, Van Soest et al., 1991) and total fatty acids (Sukhija and Palmquist, 1988). Fresh feed samples were analyzed for nitrogen by Kjeldahl method (A.O.A.C., 1984).

Blood sampling and analysis. Blood samples were drawn from the jugular vein via the catheter into 10 mL heparinized tubes (5,000 USP units of heparin/L whole blood) at 2 h preinjection, and at hourly intervals from 0 to 6 h postinjection. Plasma was harvested after centrifugation at 3,000 × g for 10 min and stored at -27°C until assayed. Plasma NEFA (Wako NEFA C kit; Wako Chem. Inc., Osaka, Japan), triglyceride (Sigma Procedure no. 336, St. Louis, MO) and glucose (Sigma Procedure no. 510, St. Louis, MO) were determined by micromethods and analyzed by using an ELISA plate reader (BioRad model 2550 EIA reader, Japan). Plasma samples analyzed for BHBA were first deproteinized and stored at -27 °C until analyzed by an established enzymatic procedure (Williamson and Mellanby, 1972). Insulin was assayed by using a radioimmunoassay kit (Coat-a-Count,® Diagnostic Products, Los Angeles, CA) and counted by using a gamma counter (Cobra 5005, Packard, Downers Grove, IL). Inter- and intra-assay coefficients of variation were 13 and 10%, respectively.

Statistical analysis. Quantity of dry matter consumed per given time, and blood measures taken over time were analyzed by the repeated measures ANOVA in a split plot design with the GLM procedure of SAS® (SAS Inst. Inc., Cary, NC). The statistical model was; Yijkl = µ + Di + Pj + Hk + DPHijk + Il + DIil + eijkl, where µ = overall mean; Di = average effect of the ith diet, I = 1, 2; Pj = average effect of the jth period, j = 1, 2; Hk = average effect of the kth heifer, k = 1, ..., 8; DPHijk = error term for Di, Pj, Hk ; Il = average effect of the lth injection, l = 1, 2; DIil = average effect of interaction between the ith diet and the lth injection; and eijkl = residual error. The whole plot effects, Di, Pj, and Hk were tested using DPHijk as the error term, and split plot effects, Il and DIil were tested using the residual error. Differences between treatment means were considered to be significant at P <=  0.05 and probability values between 0.05 and 0.10 were considered to indicate a trend toward a significant effect. Because of high ambient temperature (mean daily high 27 ± 3.1°C), two heifers in the low fat diet + MA injection treatment group went off feed in Period 1; therefore, two observations were missing in data analysis.

RESULTS

Feed intake. Cumulative dry matter intake and quantity of dry matter consumed are in Figure 1 and Table 2, respectively. A diet by injection interaction effect was not found in either measure. The high fat diet tended to decrease quantity of dry matter consumed during -2 to 0 h postinjection (low fat diet 1.78 vs. high fat diet 1.42 kg, SEM = 0.10, P = 0.07) and during -2 to 22 h (low fat diet 8.50 vs. high fat diet 7.68 kg, SEM = 0.17, P = 0.1) when compared to the low fat diet (Table 2). Mercaptoacetate injection depressed quantities of dry matter consumed during 0 to 2 and 2 to 4 h after its injection (P < 0.0004 and <0.0003, respectively) without influencing 24 h dry matter intake. The high fat diet also decreased the amount of dry matter eaten during 2 to 4 h postinjection (P = 0.01). Compensatory intake occurred in the group injected with MA as time proceeded.
Fig. 1. Cumulative dry matter (DM) intake by dairy heifers fed low or high fat diets before and after intravenous injections of saline or 0.15 mol/L sodium mercaptoacetate (300 µmol/kg body weight0.75). Legends are LS = low fat diet + saline, LM = low fat diet + sodium mercaptoacetate, HS = high fat diet + saline, and HM = high fat diet + sodium mercaptoacetate. Feeding was at -2 h. Values are means ± SEM (n = 2 for LM and n = 4 for other treatments). No interaction between diet and injection was observed. Overall diet effect was P = 0.1. A time by injection interaction effect was P = 0.0001 without a 3-way interaction effect of time, diet and injection.
[View Larger Version of this Image (20K GIF file)]

Table 2. Quantity of dry matter consumed per given time before and after intravenous injections of saline or 0.15 mol/L sodium mercaptoacetate (300 µmol/kg body weight0.75) to dairy heifers fed low or high fat diets

[View Table]

Plasma measures. Plasma NEFA concentration (Fig. 2) was affected by both diet and injection without an interaction effect. The high fat diet increased pre- and postfeeding plasma NEFA concentrations when compared to the low fat diet (P = 0.0003 and = 0.0006, respectively). A time by injection interaction effect was observed in plasma NEFA concentration (P < 0.04); MA injection increased plasma NEFA concentration immediately after its injection with a peak at 2 h postinjection, after which a prompt decrease in plasma NEFA concentration followed. A continuous decrease in plasma NEFA concentration occurred in saline-treated groups after feeding.
Fig. 2. Changes in plasma nonesterified fatty acid (NEFA) concentrations in dairy heifers fed low or high fat diets before and after intravenous injections of saline or 0.15 mol/L sodium mercaptoacetate (300 µmol/kg body weight0.75). Legends are LS = low fat diet + saline, LM = low fat diet + sodium mercaptoacetate, HS = high fat diet + saline, and HM = high fat diet + sodium mercaptoacetate. Feeding was at -2 h. Values are means ± SEM (n = 2 for LM and n = 4 for other treatments). No interaction between diet and injection or 3-way interaction of time, diet and injection were observed. Overall diet effects were P = 0.0001 and = 0.0003 pre- and postinjection, respectively. A time by injection interaction effect was P < 0.004.
[View Larger Version of this Image (21K GIF file)]

Plasma BHBA concentration (Fig. 3) rapidly increased up to 2 h after feeding (P = 0.0001) and overall was higher for the low fat diet than the high fat diet (P  < 0.08) without an interaction effect of diets and injections. A marked decrease in plasma BHBA concentration occurred in the low fat group immediately after injection of MA up to 2 h postinjection (P  < 0.06). A time by diet interaction was observed (P = 0.02). In the high fat diet groups, plasma BHBA concentration increased up to 3 h postinjections and reached a plateau. In the low fat diet groups, plasma BHBA concentration decreased up to 2 h postinjection and increased gradually from 3 h postinjection.

Fig. 3. Changes in plasma beta -hydroxybutyrate (BHBA) concentrations in dairy heifers fed low or high fat diets before and after intravenous injections of saline or 0.15 mol/L sodium mercaptoacetate (300 µmol/kg body weight3/4). Legends are LS = low fat diet + saline, LM = low fat diet + sodium mercaptoacetate, HS = high fat diet + saline, and HM = high fat diet + sodium mercaptoacetate. Feeding was at -2 h. Values are means ± SEM (n = 2 for LM and n = 4 for other treatments). Interaction between diet and injection or 3-way interaction of time, diet and injection were not observed. Time by diet and time by injection interactions were P = 0.02 and = 0.1, respectively.
[View Larger Version of this Image (22K GIF file)]

Plasma triglyceride concentration (Figure 4) was increased by the high fat diet before and after injection (P = 0.0001 and < 0.02, respectively). Mercaptoacetate significantly decreased plasma TG concentrations up to 5 h after injection.

Fig. 4. Changes in plasma triglyceride concentrations in dairy heifers fed low or high fat diets before and after intravenous injections of saline or 0.15 mol/L sodium mercaptoacetate (300 µmol/kg body weight0.75). Legends are LS = low fat diet + saline, LM = low fat diet + sodium mercaptoacetate, HS = high fat diet + saline, and HM = high fat diet + sodium mercaptoacetate. Feeding was at -2 h. Values are means ± SEM (n = 2 for LM and n = 4 for other treatments). No interaction among factors were observed. Overall diet effects were P = 0.0001 and < 0.02 pre- and postinjection, respectively.
[View Larger Version of this Image (22K GIF file)]

Plasma glucose concentration (Figure 5) was not influenced by diets but increased with time (P = 0.0002). There was a time by injection interaction effect on plasma glucose concentration; MA elevated (P = 0.008) plasma glucose at 2 and 3 h after injection while saline did not alter plasma glucose levels.

Fig. 5. Changes in plasma glucose concentrations in dairy heifers fed low or high fat diets before and after intravenous injections of saline or 0.15 mol/L sodium mercaptoacetate (300 µmol/kg body weight0.75). Legends are LS = low fat diet + saline, LM = low fat diet + sodium mercaptoacetate, HS = high fat diet + saline, and HM = high fat diet + sodium mercaptoacetate. Feeding was at -2 h. Values are means ± SEM (n = 2 for LM and n = 4 for other treatments). No interaction between diet and injection or 3-way interaction of time, diet and injection were observed. Overall diet effect was not significant. A time by injection interaction effect was P = 0.008.
[View Larger Version of this Image (20K GIF file)]

Plasma insulin concentration (Figure 6) tended to be lowered by the high fat diet (P = 0.1). A rapid decrease in plasma insulin occurred in response to MA injection (P = 0.0001).

Fig. 6. Changes in plasma insulin concentrations in dairy heifers fed low or high fat diets before and after intravenous injections of saline or 0.15 mol/L sodium mercaptoacetate (300 µmol/kg body weight0.75). Legends are LS = low fat diet + saline, LM = low fat diet + sodium mercaptoacetate, HS = high fat diet + saline, and HM = high fat diet + sodium mercaptoacetate. Feeding was at -2 h. Values are means ± SEM (n = 2 for LM and n = 4 for other treatments). No interaction among factors were observed. Overall diet effect was not significant. Overall injection effect was P = 0.0001.
[View Larger Version of this Image (19K GIF file)]

DISCUSSION

Inhibition of fatty acid oxidation by MA did not reverse fat-induced depression of feed intake in dairy cattle fed a high fat diet. Instead, MA depressed feed intake for several hours. It was suggested that reducing equivalents produced from fatty acid oxidation may mediate feed intake depression in ruminants fed high fat diets (Emery et al. 1992). Mercaptoacetate inhibits fatty acid oxidation by inhibiting mitochondrial acyl-CoA dehydrogenases (Bauché et al. 1981), which should decrease generation of reducing equivalents and stimulate food intake if the hypothesis is true. Inhibition of fatty acid oxidation by mercaptoacetate (Scharrer and Langhans 1986, Singer and Ritter 1994) or methyl palmoxirate (Friedman et al. 1986) increased food intake in rats fed diets rich in fat. Mercaptoacetate increased plasma NEFA and decreased plasma BHBA concentrations in this study, consistent with the previous study (Scharrer and Langhans 1986). Although the inverse relationship between plasma NEFA and BHBA concentrations suggests that fatty acid oxidation was inhibited by MA injection, the feed intake response was completely opposite to studies in rats (Friedman et al. 1986, Scharrer and Langhans 1986, Singer and Ritter 1994).

The cause of decreased feed intake due to MA injection in this study is uncertain. No signs of discomfort or toxicity were detected in the cattle, and rectal temperature and behavior were normal after MA injection. In rats, no side effects were reported even when MA was administered intravenously at 600 µmol/kg body weight (Van Dijk et al. 1995). Metabolic disturbances provoked by inhibition of fatty acid oxidation or other effects elicited by MA directly could have resulted in decreased food intake. Other studies suggested that whether or not inhibition of fatty acid oxidation affects feeding may depend on the metabolic status of animals. Inhibitors of fatty acid oxidation stimulated food intake in rats fed medium or high fat diets but not a low fat diet (Friedman et al. 1986, Scharrer and Langhans 1986). Also MA increased food intake by rats more during the light phase than during the dark phase, possibly because of higher fatty acid oxidation during the light phase (Scharrer and Langhans 1986).

During the process of evolution, ruminants adapted to feedstuffs low in fat so that their dependence on fat as a fuel is much less than nonruminants. Only in negative energy balance does mobilized fat become a major energy substrate in ruminants (Palmquist 1994). In the fed condition, short-chain fatty acids produced by microbial fermentation of feed in the rumen are the predominant energy sources, as was the case for the animals in this study. Feeding animals to partial satiation before MA injection should shift their energy source from long-chain fatty acids to short-chain fatty acids, thereby reducing the role of long-chain fatty acid oxidation as a mediator of feed intake regulation.

The MA-induced depression of feed intake remains unexplained. In a recent study, intravenous MA injection increased plasma norepinephrine in rats (Van Dijk et al. 1995). This alpha -adrenoceptor agonist serves as a hunger signal during the light phase, whereas it acts as a satiety signal during the dark phase in rats (Margules et al. 1972). Therefore, it can not be ruled out that the appetite-stimulatory effect of MA also may have been associated with an increase in plasma norepinephrine in the previously reported studies (Friedman et al. 1986, Scharrer and Langhans 1986, Singer and Ritter 1994). In those studies, MA had less potent and shorter stimulatory effects on food intake in rats during the dark phase than during the light phase (Scharrer and Langhans 1986), possibly attributable to the satiety effect of norepinephrine released by MA injection. A hypothalamic injection of l-norepinephrine elicited feeding in sheep (Baile et al. 1972, 1974). However, unlike sheep and rats, l-norepinephrine suppressed feed intake in cattle (Baile et al. 1972). There could be different physiological roles of the alpha -adrenoceptor agonist in satiety regulation between sheep and cattle. Although no measurement was made, norepinephrine may have been a factor in the MA-induced depression of feed intake in this study.

Plasma insulin and metabolite measures. Plasma insulin and lipid metabolite concentrations were influenced by both diet and MA injection. Plasma insulin concentration was lowered by feeding fat, consistent with the previous study (Choi and Palmquist 1995). Mercaptoacetate profoundly lowered plasma insulin, which supports the observation in rats (Van Dijk et al. 1995). Norepinephrine release, noted above, may cause alpha -adrenoceptor-mediated decrease of insulin production by the pancreatic beta -cell (Edwards 1986). However, decreased food intake could have decreased plasma insulin. In lactating cows high fat diets depressed feed intake, and that caused lowered plasma insulin concentrations (Choi and Palmquist 1995). Response of plasma insulin to altered feed intake is immediate in ruminants because of rapid production of propionate, a potent insulin secretagogue, in the presence of dietary carbohydrate in the rumen (Grovum 1995).

Plasma glucose concentration was not influenced by diet but was increased by MA injection. The decreased plasma insulin could have increased plasma glucose concentration. It also is likely that an alpha 2-adrenoceptor-mediated stimulation of hepatic glycogenolysis by norepinephrine contributed to increased plasma glucose concentration in the MA-treated group (Van Dijk et al. 1995).

High fat diets usually cause increased plasma NEFA and triglyceride concentrations in dairy cattle (Choi and Palmquist 1995). Mercaptoacetate appeared to increase plasma NEFA by inhibiting fatty acid oxidation and reesterification, and by stimulating fatty acid mobilization (Sabourault et al. 1977). Plasma NEFA concentration may increase when insulin is decreased, because of the antilipolytic effect of insulin in adipose tissue (Vernon 1988). Also, MA-stimulated norepinephrine secretion would stimulate lipolysis in adipose tissue (Van Dijk et al. 1995). Plasma triglyceride concentration was decreased by MA injection in animals fed the high fat diet, which may have resulted from lower fat absorption as a consequence of decreased feed intake. Perhaps MA itself decreased intestinal fat absorption via norepinephrine, in that stimulation of intrapancreatic adrenergic nerves inhibited pancreatic enzyme secretion (Kato et al. 1991), thereby decreasing fat digestion.

Although MA undoubtedly decreased plasma BHBA concentration, it is not certain whether the decrease was due to inhibition of fatty acid oxidation by MA or due to decreased feed intake and lower ruminal butyrate production. Should the high fat diets increase fatty acid oxidation in the liver, plasma BHBA concentration would be increased. However, overall plasma BHBA concentration apparently reflected feed intake in that it decreased as feed intake decreased in animals fed the high fat diet. In ruminants, plasma BHBA concentration is influenced by two origins: plasma NEFA oxidation in the liver (Pethick et al. 1984) and oxidation in the ruminal wall of butyrate produced by carbohydrate-fermenting rumen microbes (Stevens and Stettler 1966). Despite similar feed intakes of the high and the low fat diets, a greater reduction of plasma BHBA concentration occurred for the low fat diet rather than for the high fat diet when MA was injected. Changes in ruminal butyrate production per unit change in feed intake should be greater for the low fat diet because it contained a greater amount of fermentable carbohydrate than did the high fat diet. Measurement of plasma BHBA concentration as an index of fatty acid oxidation may not be useful in ruminants in which the plasma BHBA pool also is influenced by ruminal fermentation of dietary carbohydrate. It was not possible to separate direct effects of MA from effects of feed intake on plasma NEFA and BHBA because MA injection decreased feed intake.

These data show that intravenous MA injection depresses feed intake in ruminants and thus it is not a useful probe to study the mechanism of feed intake regulation in dairy cattle fed fat. Measurement of plasma BHBA concentration to monitor the extent of fatty acid oxidation in vivo is not useful in ruminants because of its dual origin. Studies on the role of MA in norepinephrine secretion and the role of norepinephrine in the MA-induced depression of feed intake should be useful.

FOOTNOTES

1   Support provided by state and federal funds appropriated to the Ohio Agricultural Research and Development Center, The Ohio State University. Manuscript no. 52-96. 
2   The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.
3   To whom correspondence should be addressed.
4   Abbreviations used: BHBA, beta -hydroxybutyrate; MA, mercaptoacetate; NEFA, non-esterified fatty acid.

Manuscript received 15 April 1996. Initial reviews completed 18 June 1996. Revision accepted 16 September 1996.

ACKNOWLEDGMENTS

Authors gratefully thank Michael S. Allen's staff at Michigan State University and Ramon Casals, visiting scholar at The Ohio State University, for their technical assistance during this experiment. Appreciation also is extended to Bert Bishop, OARDC, for his statistical advice.

LITERATURE CITED

0022-3166/97 $3.00 ©1997 American Society for Nutritional Sciences



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