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Feeding Rumen-Inert Fats Differing in Their Degree of Saturation Decreases Intake and Increases Plasma Concentrations of Gut Peptides in Lactating Dairy Cows

Department of Animal Sciences, The Ohio State University, Ohio Agricultural Research and Development Center, 1680 Madison Ave., Wooster 44691-4096

¹ Corresponding author: c.k.reynolds{at}reading.ac.uk

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ACKNOWLEDGEMENTS REFERENCES

 
Our objective was to determine the effect of feeding rumen-inert fats differing in their degree of saturation on dry matter intake (DMI), milk production, and plasma concentrations of insulin, glucagon-like peptide 1 (7–36) amide (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and cholecystokinin (CCK) in lactating dairy cows. Four midlactation, primiparous Holstein cows were used in a 4 x 4 Latin square experiment with 2-wk periods. Cows were fed a control mixed ration ad libitum, and treatments were the dietary addition (3.5% of ration dry matter) of 3 rumen-inert fats as sources of mostly saturated fatty acids (SFA), monounsaturated fatty acids (MUFA), or polyunsaturated fatty acids (PUFA). Daily DMI, milk yield, and composition were measured on the last 4 d of each period. Jugular vein blood was collected every 30 min over a 7-h period on d 12 and 14 of each period for analysis of plasma concentrations of hormones, glucose, and nonesterified fatty acids. Feeding fat decreased DMI, and the decrease tended to be greater for MUFA and PUFA compared with SFA. Plasma concentration of GLP-1 increased when fat was fed and was greater for MUFA and PUFA. Feeding fat increased plasma glucose-dependent insulinotropic polypeptide and CCK concentrations and decreased plasma insulin concentration. Plasma CCK concentration was greater for MUFA and PUFA than for SFA and was greater for MUFA than PUFA. Decreases in DMI in cows fed fat were associated with increased plasma concentrations of GLP-1 and CCK and a decreased insulin concentration. The role of these peptides in regulating DMI in cattle fed fat requires further investigation.

Key Words: gut peptide • dietary fat • saturation • intake

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ACKNOWLEDGEMENTS REFERENCES

 
Dry matter intake, and particularly energy intake, is a critical determinant of milk production. When DMI is limited in high-producing dairy cows, increasing the NE_L concentration of the diet is one approach that can improve energy intake. The addition of fat is a common practice in the dairy industry; however, increasing the concentration of fat in the diet often decreases DMI (Allen, 2000). The response of DMI to dietary fat varies because of a number of factors, including the stage of lactation, basal diet, and amount and type of fat fed (Firkins and Eastridge, 1994). A number of studies have shown that the type of fat (e.g., FFA or triglycerides) and degree of saturation determine the extent that dietary fat reduces DMI (Schauff and Clark, 1992; Benson et al., 2001; Litherland et al., 2005). The mechanisms by which dietary fat reduces DMI are not completely understood, but gut peptides such as glucagon-like peptide 1 (7–36) amide (GLP-1) and cholecystokinin-8 (CCK), among others, have been postulated as mediators in the regulation of appetite and feed intake in lactating dairy cows (Choi et al., 2000; Ingvartsen and Andersen, 2000; Benson and Reynolds, 2001).

Glucose-dependent insulinotropic peptide (GIP) and GLP-1 are peptides of gut origin that increase the secretion of insulin in nonruminants under certain conditions (Holst, 1997), thus potentially regulating DMI via an increase in insulin concentration and effects on neuropeptide Y in the hypothalamus (Gale et al., 2004). Effects of GIP on insulin secretion are both direct, through stimulation of the ß-cells of the pancreas (Knapper et al., 1996), and indirect, through positive effects on GLP-1 secretion from the L-cells of the distal small intestine (Damholt et al., 1998). Glucagon-like peptide-1 (7–36) amide is also a potential regulator of DMI through inhibitory effects on gut motility and direct effects on the hypothalamus (Shimizu et al., 1987; Turton et al., 1996; Holst, 1997). Because of the digestive and physiological differences between ruminants and nonruminants with regard to nutrient absorption and metabolism, the role of GIP and GLP-1 in the regulation of insulin and appetite in dairy cows is not clearly understood. However, a reduction in gut motility caused by the action of GLP-1 could increase rumen fill and physically restrict feed intake. In lactating dairy cows, abomasal infusion of fat increased plasma concentration of GLP-1 and decreased DMI (Benson and Reynolds, 2001; Litherland et al., 2005). Effects of dietary or intragastrically infused fat on the secretion or plasma concentration of GIP have not been reported for cattle, but in preruminant goats, feeding full-fat milk or milk fat increased plasma GIP concentration (Martin et al., 1993). In nonruminants, dietary fat stimulates GIP secretion, but the effect on plasma concentration is more pronounced when dietary fat is consumed with glucose (Knapper et al., 1996).

As with GLP-1, CCK may decrease DMI by decreasing gut motility (Kumar et al., 2004). Although CCK plays a role in the regulation of meal size, total DMI is often not reduced in either nonruminants (Moran, 2004) or cattle (Choi et al., 2000) because of a corresponding increase in the number of meals. Effects of dietary fat on plasma concentration of CCK in ruminants are equivocal. Choi and Palmquist (1996) reported a CCK concentration response in dairy cows fed high-fat diets [calcium salts of palm fatty acids (FA); 9% of DMI], but the effects of including smaller amounts of dietary fat were not significant. In contrast, feeding canola oil (1 kg/d) increased plasma CCK concentration but did not reduce DMI, whereas abomasal infusion of the same amount of canola oil both reduced DMI and increased plasma CCK concentration (Chelikani et al., 2004). In other studies, infusion of fat (vegetable oil) into the abomasum decreased DMI but did not increase plasma CCK concentration (Benson and Reynolds, 2001; Litherland et al., 2005). These observations suggest that the DMI depression in cows fed supplemental fats may be mediated through increased secretion of these gut peptides and subsequent effects on gut motility, insulin secretion, and the hypothalamus. Therefore, the objective of the present study was to determine the extent to which the degree of saturation of supplemental rumen-inert fat would affect DMI and plasma concentrations of GLP-1, CCK, GIP, and insulin in lactating dairy cows.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ACKNOWLEDGEMENTS REFERENCES

 
Animals and Diets
All animal procedures were approved by the Agricultural Animal Care and Use Committee of The Ohio State University. For 4 wk before the start of the study, 4 primiparous Holstein cows (averaging 614 kg of BW, 165 ± 9 DIM, and 34.4 ± 0.7 kg/d of milk yield at the start of the trial) were fed a control diet (Table 1) of a mixed ration formulated to meet nutrient requirements (NRC, 2001). The formulation of the control diet was based on the ration that was fed to the cows immediately before they were used for the present study. Cows were housed in individual tie stalls with water cups and were milked at 0130 and 1300 h in the herd parlor. Daily rations were provided at 0800 h, and cows were fed ad libitum (10% refusal). Ration composition was adjusted weekly for changes in component DM concentration.

Measurements
Dry matter intake and milk yield and composition were measured for the last 4 d of each period, as described by Beckman and Weiss (2005). Feed samples were taken weekly and pooled for each period and analyzed for DM (100°C), ash (600°C), Kjeldahl N, starch, NDF, and total FA (Table 1), as described by Beckman and Weiss (2005). The FA profile of the diets fed is presented in Table 2. A milk sample preserved with bronopol was stored at 2°C until analyzed for fat, lactose, and protein concentrations using infrared analysis (DHI Cooperative, Columbus, OH). Milk fat from samples taken from the last 2 milkings of each period was separated by centrifugation for 30 min (20,000 x g at 4°C) and stored frozen at –80°C until constituent FA were converted to methyl esters and relative concentrations determined by GLC, as described previously (Kramer et al., 1997; Reveneau et al., 2005).

Hormone and Metabolite Analysis
Concentrations of insulin, GLP-1, GIP, and CCK were measured using double-antibody RIA. The intraassay coefficients were less than 10% for insulin, 6% for GLP-1, 11% for GIP, and 4% for CCK. Plasma insulin concentration was measured using an equilibrium assay based on the assay described by Reynolds et al. (1989). Sensitivity of the insulin assay (the concentration at which bound counts were 90% of binding for the zero standard) was 0.0027 pmol/tube. Plasma GLP-1 concentration was measured using a disequilibrium assay based on the assay described by Benson and Reynolds (2001). Sensitivity of the GLP-1 assay was 0.001 pmol/tube. Plasma GIP concentration was measured much as described by Morgan et al. (1978) using a disequilibrium assay with 24- and 48-h incubations before addition of labeled GIP (#T-027-02; Phoenix Pharmaceutical, Inc., Belmont, CA) and secondary antibody (goat anti-rabbit IgG, AB21; Chemicon International, Temecula, CA), respectively. The anti-human GIP (Rab-027-02; Phoenix Pharmaceutical, Inc.) has 100% cross-reactivity with human and porcine GIP. Serial addition of bovine plasma displaced labeled GIP linearly, with a slope similar to the displacement by porcine standards. Sensitivity of the GIP assay was 0.025 pmol/tube. Plasma CCK concentration was measured in extracted plasma using a commercial disequilibrium assay (Euro-Diagnostica, Malmö, Sweden), as described by Benson and Reynolds (2001). Plasma (500 µL) was extracted with 96% ethanol (1 mL) and then centrifuged at 1,700 x g for 15 min at 4°C. The supernatant was decanted to another tube, evaporated in a freeze-dryer overnight, and then reconstituted in assay buffer before analysis. Sensitivity of the CCK assay was 0.0006 pmol/tube. Plasma glucose concentration was measured using an enzymatic assay (#1070 Glucose Trinder Assay; Stanbio Laboratory, Boerne, TX). Plasma NEFA concentration was measured using an enzymatic assay (Wako Chemicals USA, Inc., Richmond, VA) as described by Johnson and Peters (1993).

Statistical Analysis
Because of a mistake in feeding the CaSoy diet in the first period, data from one animal fed this diet were excluded from the statistical analysis. Thus, one observation was missing from the 16 possible cow and period combinations. Data for DMI and milk production and composition were averaged for each cow-period (n = 15) and analyzed using the MIXED procedure of SAS (SAS Institute, 2000) with a model testing the random effects of animal and period and the fixed effect of diet. Cows were sampled on 2 d at the end of each period to account for variation in plasma concentrations of hormones over time and to provide a more robust measurement of any postprandial responses. Hormone and metabolite concentrations were averaged for each time point across d 12 and 14 and analyzed as repeated measures over sampling times using the MIXED procedure of SAS (SAS Institute, 2000). The model used tested the random effects of animal and period and the fixed effects of diet and sampling time. Data were analyzed using the structure giving the best fit based on Akaike’s information criterion (Littell et al., 1996). Treatment means were separated using orthogonal contrasts to partition treatment sums of squares into the following comparisons: control vs. supplemental fat (control vs. EB, EnerG-II, and CaSoy), SFA vs. unsaturated fat (EB vs. EnerG-II and CaSoy) and MUFA vs. PUFA (EnerG-II vs. CaSoy).

	RESULTS

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DMI, Milk Yield, and Milk Composition
Feeding supplemental fat decreased (P < 0.05) DMI (Table 3), and the effect was numerically greater (P < 0.12) for MUFA and PUFA (Table 3) than for SFA. There was no overall effect of diet on estimated ME intake or milk yield, but MUFA and PUFA tended (P < 0.11) to decrease milk yield compared with SFA. The milk fat percentage and yield were affected by feeding fat (P < 0.06 and P < 0.04, respectively) because of a decrease when PUFA were fed (P < 0.09 compared with MUFA) and an increase when SFA were fed (P < 0.03 compared with MUFA and PUFA; Table 3). There was no effect of diet on milk protein concentration and yield, but feeding MUFA and PUFA decreased milk lactose percentage and yield (P < 0.05 and P < 0.06, respectively) compared with SFA (Table 3).

View larger version (20K): [in this window] [in a new window]   Figure 1. Plasma concentrations of glucose, glucagon-like peptide 1 (7–36) amide (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), NEFA, cholecystokinin (CCK), and insulin during a 7-h sampling period for midlactation dairy cows fed a control diet () or a diet with supplemental fat containing either mostly saturated (), mostly monounsaturated (x), or mostly polyunsaturated () fatty acids. Cows were fed immediately after sampling at 0800 h.

	DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ACKNOWLEDGEMENTS REFERENCES

Milk FA concentrations were measured as an indicator of the relative changes achieved in the profile of FA absorbed by feeding the rumen-inert fat supplements used in the present study. The responses observed are typical of other studies in which these or similar fat supplements were fed to lactating dairy cows (for a review see, e.g., Palmquist, 2006). Reductions in the concentration of short- and medium-chain SFA, although relatively small in magnitude (Table 4), are often observed when fats are fed or abomasally infused and the concentrations of longer-chain FA are increased (Drackley et al., 1992; Palmquist, 2006). The increased concentration of 16:0 when SFA and MUFA were fed reflects the content (39 to 50%) of this FA in the fat supplements fed for these treatments. Changes in the relative concentrations of trans-18:1 isomers and CLA indicate that the CaSoy product was less protected from ruminal biohydrogenation than the other supplements fed; however, the increased milk fat concentration of cis-9, cis-12 18:2 indicates that a greater absorption of this FA occurred when PUFA were fed compared with the other treatments. Previous studies have reported the extent of biohydrogenation of dietary FA when the same or similar supplemental fats were fed to ruminants. Although the unsaturated FA in EB can be subjected to biohydrogenation, the unsaturated FA content of this product is typically low (less then 15%; Grummer et al., 1996). Calcium salts of FA can also be subject to ruminal biohydrogenation, depending on the dissociation constants of their component FA, the type of ration fed, and other factors influencing rumen environment and pH (Sukhija and Palmquist, 1990). In lactating dairy cows fed supplemental EB or calcium salts of palm oil (Harvatine and Allen, 2006), the extent of biohydrogenation of total dietary cis-9, cis-12 18:2 was 84.5 and 86.6%, respectively, whereas the biohydrogenation of cis-9 18:1 was 71.5 and 63.6%, respectively. Lundy et al. (2004) also reported extensive biohydrogenation of unsaturated FA in diets supplemented with calcium salts of soybean oil FA that were fed to lactating dairy cows (77.9% of cis-9 18:1 and 92.2% of cis-9, cis-12 18:2), but they also observed a marked increase in cis-9, cis-12 18:2 flow to the omasum (from 25 to 39 g/d).

Gut Hormones, Insulin, and Metabolites
In the present study, a postprandial increase in plasma concentrations of insulin, GLP-1, GIP, and CCK was observed after feeding (Figure 1), but the increase was relatively small for GLP-1. A postprandial increase in arterial insulin concentration was reported previously in dairy cows (Choi and Palmquist, 1996; Choi et al., 2000; Benson and Reynolds, 2001). In the study by Benson and Reynolds (2001), an increased insulin concentration accompanied an increase in net VFA and glucose absorption across the portal-drained viscera (Benson et al., 2002), indicating a response of insulin secretion to increased postprandial nutrient absorption and glucose supply. A postprandial increase in the arterial concentration of GLP-1 was not observed by Benson and Reynolds (2001), but in their study, cows were fed daily rations in 3 equal meals and supplemental fat was infused continuously. In the present study, cows were fed their rations and supplemental fat once daily, and numerical increases in plasma GLP-1 and GIP concentrations over the course of the sampling period were less when control diets were fed (Figure 1). The post-prandial increase in plasma CCK concentration observed in the present study may be due to increased digesta flow and nutrient absorption from the small intestine, stimulating intestinal K cells to secrete CCK; however, a postprandial increase in plasma CCK concentration was not observed in previous studies in which lactating dairy cows were fed once daily (Choi and Palmquist, 1996; Choi et al., 2000; Chelikani et al., 2004). In the present study, the highest CCK concentration was observed after the afternoon milking at 1300 h (Figure 1), but Samuelsson et al. (1996) observed no effect of milking or feeding on plasma CCK concentration.

Plasma GLP-1 concentration increased when supplemental fat was fed, and the increase was greater when the fat fed was less saturated, but the responses to MUFA and PUFA fat sources were similar. Our results differ from those of Beysen et al. (2002), who reported that in humans, MUFA are a more potent secretagogue for GLP-1 than are PUFA; however, Thomsen et al. (1999) reported no difference in plasma concentration of GLP-1 in humans after a single meal of a food rich in SFA compared with MUFA. Nevertheless, the length of the treatment period may be important because the response of plasma GLP-1 concentration to an increased intestinal supply of FA may differ over time, that is, an acute (hours) vs. chronic (days) response. The mechanism by which GLP-1 secretion is regulated by dietary FA is not clearly understood; however, Hirasawa et al. (2005) suggested that this regulation is via a G protein-coupled receptor (GPR120) for unsaturated FA in the cells of the small intestine. Damholt et al. (1998) reported that GIP is a secretagogue for GLP-1, but in the present study differences in the response of plasma concentration of GLP-1 to the type of fat fed could not be attributed to changes in plasma GIP concentration. Plasma GIP concentration increased when fat was added to the diet, but there was no significant difference in responses across the fat supplements. In contrast, Thomsen et al. (1999) reported a difference in the response of GIP concentration when FA differing in degree of saturation were fed to humans. In that study, subjects fed MUFA had a greater plasma concentration of GIP than when mostly SFA were fed.

The decrease in insulin concentration observed when supplemental fat was fed was associated with decreased DMI, which would decrease the absorption of insulin secretagogues such as glucose and propionate. There seemed to be no relationship between changes in the concentrations of insulin and the incretin hormones GLP-1 and GIP. In the present study, plasma concentration of glucose was less than 4.5 mM, which is the concentration proposed by Holst (1997) as the threshold for GLP-1 and GIP to stimulate insulin secretion in humans. Faulkner and Martin (1999) reported an increased plasma insulin concentration in lactating sheep when GLP-1 was intravenously infused with glucose, and a plasma glucose concentration of 4.78 mM was observed in the jugular vein, but an increase in insulin concentration was not observed when GLP-1 was infused without glucose and plasma glucose concentration was 3.24 mM.

In contrast to other studies in which fat was added to the diet (Choi and Palmquist, 1996) or infused into the abomasum (Benson and Reynolds, 2001; Litherland et al., 2005), plasma CCK concentration increased with the addition of fat to diets in our study. However, Chelikani et al. (2004) found that abomasal infusion and dietary inclusion of relatively large amounts (1 kg) of canola oil, which is high in MUFA, increased intestinal CCK mRNA expression and plasma concentrations of CCK in lactating dairy cows. In addition, Harvatine and Allen (2005) reported that feeding lactating dairy cows fats high in unsaturated FA increased plasma CCK concentration compared with feeding a fat high in SFA. These data and the results of the present study indicate that the response of plasma CCK concentration is influenced by the relative amounts of unsaturated FA reaching the small intestine, which is similar to findings in humans (Robertson et al., 2002). Differences in plasma CCK response to supplemental fats provided by postruminal infusion (Benson and Reynolds, 2001; Litherland et al., 2005), compared with the present study in which supplemental fat was fed, may be due to differences in the timing of supplemental FA delivery to the small intestine (constant infusion vs. postprandial increase).

The reason for a greater response of plasma CCK concentration to feeding MUFA vs. PUFA is not clearly understood, but it might be a consequence of ruminal biohydrogenation of the PUFA in CaSoy. Although differences in milk FA profile indicate that rumen biohydrogenation occurred, a better understanding of the profile and amount of FA absorbed by the small intestine is needed to explain our results. In the study by Chelikani et al. (2004), feeding canola oil increased plasma CCK concentration but did not reduce DMI. Our assumption was that the increase in CCK concentration observed was more important for gut function and motility (Kumar et al., 2004) and exocrine pancreatic secretion (Tachibana et al., 1995), which would benefit nutrient digestion and especially fat digestion, and could in part explain why SFA are less digestible than unsaturated FA (Firkins and Eastridge, 1994).

The increase in NEFA concentration when fat was fed may be explained by an increase in fat absorption along with a decrease in insulin concentration, which could allow for more lipolysis in adipose tissue. In the present study, plasma NEFA concentrations were lower in cows fed SFA vs. unsaturated FA, which agrees with the results of studies showing that dietary SFA decrease lipolysis in rats to a greater extent than do dietary PUFA (Awad and Chattopadhyay, 1986).

In conclusion, the decrease in DMI observed when supplemental fat was fed was associated with an increase in plasma concentration of GLP-1. This gut peptide hormone has hypophagic effects, and its concentration was highest when fats high in MUFA and PUFA were fed and DMI was lowest. In present study, we did not observe an increase in plasma insulin concentration when increases in plasma GIP and GLP-1 were observed; however, glucose concentration, which modulates insulin secretion, was always below the threshold value of 4.5 mM proposed by Holst (1997) as required for these gut peptides to have positive effect on insulin secretion in humans. In contrast to previous studies in our laboratory in which supplemental fat was infused postruminally, in the present study plasma concentration of CCK increased when supplemental fat was fed, and the response of plasma CCK to dietary fat was greatest when the fat source was high in MUFA. Results of the present and previous studies implicate GLP-1, or other cosecreted products of proglucagon processing (e.g., oxyntomodulin or GLP-2), as potential mediators of the effects of dietary fat on DMI in lactating dairy cows. Further research is needed to understand the mechanisms by which dietary FA regulate the secretion of gut peptides, the interactions of these hormones, and their effects on gut function and DMI in dairy cattle.

	ACKNOWLEDGEMENTS

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Our sincere appreciation is extended to D. Luchini of NutriSciences for providing the EnerG-II and calcium salts of soy FA fed in the present study. We are grateful to K. Miller and the staff of the Ohio Agricultural Research and Development Center, Krauss Dairy Center, for assistance with animal care and feeding and to L. Winkelman, V. Cannon, and C. V. D. M. Ribeiro for technical assistance. A. E. Relling was supported by grants provided by Bunge y Born Foundation and The Fulbright Foundation. Salaries and research support were provided by State and Federal funds appropriated to the Ohio Agricultural Research and Development Center, The Ohio State University (manuscript no. 22-06AS).

	FOOTNOTES

 
² Present address: School of Agriculture, Policy and Development, The University of Reading, PO Box 237, Earley Gate, Reading, RG6 6AR, UK.

Received for publication August 17, 2006. Accepted for publication October 19, 2006.

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TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ACKNOWLEDGEMENTS REFERENCES

 


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