Duodenal Rapeseed Oil Infusion in Early and Midlactation Cows. 3. Plasma Hormones and Mammary...

Duodenal Rapeseed Oil Infusion in Early and Midlactation Cows. 3. Plasma Homones and Mammary Apparent Uptake of Metabolites

GERARD0 GAGLIOSTRO> YVES CHILLIARD,2 and YARIEJEANNE DAVICC03 Laboratoire de la Ladation

InstlM National de la Recherche Agronomlque Theix 63122 St-GenBs Champaneb, France

ABSTRACT

Rapeseed oil was infused continu- ously (1.0 to 1.1 kg/d) into the duode- num of Holstein x Friesian multiparous cows during the first 3 wk of lactation (oil treatment, 6 cows versus 6 controls, early lactation trial) or after 100 d of lactation (midlactation trial, 9 cows in a crossover design).

In the midlactation trial, plasma glucose, 3-hydroxybutyrate, and free glycerol were not affected by oil infusion. Postprandial plasma NEFA were higher in oil-infused than in control cows; plasma triglycerides, phospholipids, and cholesterol were significantly increased in oil treatment. Plasma insulin was lower and somatotropin higher in oil-infused cows, whereas insulin-like growth factor-I and triiodothyronine were not affected.

During the early lactation trial, there were few significant effects of oil infusion on measured plasma metabolites and hormones. Preprandial glucose and NEFA were lower in oil treatment during wk 2, preprandial phospholipids were higher in wk 1 and 3, and free cholesterol was higher in wk 1.

Responses of plasma glucose and NEFA to insulin challenge were not clearly affected by oil treatment during either trial. Differences in plasma triglycerides between jugular and mammary veins were higher in oil treatment in both trials. Oil infusion did not a€fect jugular-

Received March 19, 1990. Accepted Jarmary 31, 1991. 'Present addnss: Institnto Nacional de Tccnologia

%nit6 Motabolismc Mincrat et O s t t b g t n b .

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mammary differences of other m e t a b lites except for a slight increase in cholesterol esters in midlactation. The relationships between jugular-mammary differences and jugular plasma concentrations showed that up to 24, 27, 54,

glycerides, and 3-hydroxybutyrate apparently were taken up by the mammary gland. (Key words: duodenal oil infusion, blood metabolites, blood hormones)

and 17% Of jugular glucose, NEFA, tri-

Abbreviation key: C = control treatment, IGF-I = insulin-like growth factor-I, J-M = jugular-mammary, 0 = rapeseed oil infusion treatment, ST = somatotropin, T3 = triiodothyronine, 3-HB = 3-hydroxybutyrate.

INTRODUCTION

The study of variations in concentrations of plasma metabolites and hormones can offer a useful insight into the productive and metabolic responses observed when fat is fed to lactating dairy cows. Lipid supplementation may contribute to the prevention of ketosis in early lactation by raising plasma glucose concentrations (21) and lowering ketone bodies (5, 21), although increases in plasma glucose by fat feeding were not consistently reported (5, 16, 17, 28, 33). Hormones play a major role in coordinating

the partition of dietary fatty acids among milk, adipose tissue, and oxidation in different tissues (26). Dietary fat did not seem to affect plasma somatotropin (ST) in several experi- ments (6, 12, 22,29), although decreases during early (32) and late lactation (25) also were observed. In bulls (19), fat feeding increased mean and peak ST concentrations.

Plasma insulin concentration was decreased (2, 12, 18, 27), not affected (6, 22. 29), or increased (12) by fat feeding. Because supplemental fat can increase plasma STinsulin ratio

1991 J Dairy Sci 741893-1903 1893

1894 GAGLIOSTRO ET AL.

in early lactation (26) and because higher adipose lipolysis is associated with higher plasma ST:insulin (34). dietary fat may promote changes in adipose tissue metabolism. Higher in vitro and in vivo stimulated lipolytic responses were indeed observed in rapeseed

The aim of our study was to determine the effects of duodenal infusion of rapeseed oil on plasma metabolite and hormone concentrations and mammary apparent uptake of metabolites in early and midlactation dairy cows. Glucose and NEFA responses to an insulin challenge also were studied in an attempt to correlate them to the lower milk protein content observed in oil-infused cows (13), because insulin resistance was a mechanism likely to be involved in the decreased mammary protein synthesis with fat feeding (27).

oil-infused COWS (14).

MATERIALS AND METHODS

Animals and diets have been described previously (13). Treatments were continuous duodenal infusion of rapeseed oil (0) or control (C) without infusion. In early lactation (trial l), 6 cows received 0 (1.0 kg/d) from d 17 (SD = 4) before expected calving date to d 21 postpartum, and 6 other cows received C. Jug- ular blood was taken at 0830 h (before feeding) at wk -1, 1, 2, and 3 postpartum as well as at wk 9 (postexperiment). Blood was sampled in wk 3 the day before adipose tissue was biopsied (21 f 1 of lactation) for metabolic studies (14). Mammary abdominal venous blood was sampled at wk 2 postpartum at 0830 and 1330 h (about 4.5 h after feeding); jugular blood also was taken at 1330 h at wk 2 postpartum. Immediately after the 1330-h jugular and mammary samples were taken (wk 2), insulin (Actrapid MC 40 unitdd, Novo Indus- uie Pharmaceutique, Paris, France) was in- jected intravenously (.12 unitsbg live weight), and an additional jugular blood sample was taken 30 min later. Insulin dose and sampling time after insulin were chosen accurding to Bernal-Santos' results (4).

In midlactation (trial 2), 9 multiparous Hol- stein x Friesian cows were allotled to two treatments and used in a crossover design. Mean lactation days at the beginning of peri- ods l and 2 were 100 f 14 and 142 f 14, respectively. Cows on 0 were allowed to re-

main 12 to 18 d at the maximal oil dose (1.1 kg/d) before the first blood sample was collected. Preprandial (0830 h) jugular and mammary venous blood was taken the day before adipose tissue biopsies at d 134 f 14 (period 1) and 181 f 14 (period 2) of lactation (14). Postpran- dial jugular blood was taken at 1330 h during 2 consecutive d from d 121 f 14 (period 1) and 170 f 14 (period 2) of lactation. On d 1, intravenous insulin challenge (.12 unitskg live weight) was done immediately after the 1330-h sampling, and blood also was taken 30 and 120 min later.

In both trials, blood was collected into a heparinized (5 units/ml blood) flask for metabolite analysis and into a vacutainer (Venoject; Terumo, Leuven, Belgium) containing EDTA (7 mg/5 ml blood) for hormone analysis; 30 pl of Iniprol (lo6 Kallicrein Inhibitor Unit/5 ml; Choay, Paris, France) also were added to EDTA-plasma aliquots (.6 ml) for ST and insulin-like growth factor-1 (IGF-I) detenni- nations. Blood was kept at 4'C, and plasma was obtained immediately by centrifugation (3000 x g for 15 min) and stored at -20'C until analyses using an autoanalyzer (Isamat; Isa-Biologie, Cachan, France) and commercial kits for glucose (Merckotest; Merck, Nogent- sur-Mame, France), phospholipids (B-Test; Wako, Biolyon, DardUy, France), total and free cholesterol (Boehringer Mannheim, Ger- many), and NEFA (NEPA C Test; Wako, Bi- olyon, Lyon, France). The 3-hydroxybutyrate (3-HB) was measured automatically as described by Barnouin et al. (3). The sum of glyceride plus free glycerol was determined manually using a commercial kit (Triglenzyme Color, Biotrol, Paris, France) and free glycerol as described by Wieland (35). Triglycerides were calculated as the molar difference between total and free glycerols. Plasma im- munoreactive ST and IGF-I were analyzed by radioimmunoassay (1 1). Plasma insulin and triiodothyronine (T3) were determined by radioimmunoassay using INSIK-1M RIA (Oris Industry, Gif-sur-Yvette, France) and Amerlex- M T3 radioimmunoassay kits (Amersham, Les Ulis, France), respectively.

In trial 1, statistical differences between C (n = 6) and 0 (n = 6) treatments were analyzed at each week using the Student's t test (9). Data also were analyzed as a split-plot for wk 1,2, and 3 of lactation (31). Random effect of

Journal of Dairy Science Vol. 74, No. 6, 1991

HORMONES AND METABOLITES IN OILINrmSED COWS 1895

cows nested within treatment was used as error to test treatment effect (1, 10 df). Time x cows nested within treatment interaction was used as error to test week effect and week x treatment interaction (2, 20 df).

In trial 2, differences between treatments were tested by ANOVA using the following model (9):

where p = mean; Ci = cow i (i = 1 to 9); Pj = period j (i = 1 or 2); Tk = treatment k (k = 1 or 2); and l$jk = residual. In both trials, within- treatment observations on changes in each cow [0830- vs. 1330-h samples, wk 3- vs. wk 9 samples in trial 1, jugular-mammary (J-M) vein differences in plasma metabolites, and changes in plasma metabolites after insulin challenge (n = 6, trial 1; n = 9, trial 2)] were analyzed using the pairwise t test (9) to test whether changes were different from zero. Probabilities of 1, 5 , and 10% were used,

RESULTS

Effects on Plasma Metabolites

Changing the scale of blood metabolite concentrations by logarithmic or square root trans- formations prior to ANOVA did not change the results. In midlactation (trial 2), levels of plasma glucose, 3-HB, and free glycerol were not affected by rapeseed oil infusion (Table 1). Postprandial plasma NEFA level was higher in 0 than in C cows. Preprandial and postprandial triglycerides, phospholipids, and esterified and free cholesterol were significantly increased by oil infusion.

In early lactation (trial l), preprandial but not postprandial plasma glucose level was lower in 0 at wk 2 of lactation. Levels of 3-HB, free glycerol, and triglycerides were not affected by oil infusion. Preprandial plasma NEFA level was not affected by treatment before calving (wk -1) but was higher in C during wk 2 of lactation. F'reprandial phospho- lipid level was significantly higher in 0 cows at wk 1 and 3 of lactation and free cholesterol at wk 1 postpartum.

The split-plot analysis over wk 1, 2, and 3 of lactation led basically to similar conclusions as using the t test at each week A significant

oil effect was only detected for preprandial phospholipids (C = 1.00 gL; 0 = 1.33 g/L; P < .06) and treatment x week interactions were significant for 3-HB (P < .lo) and phospholipids (P < .oQ) only. Time effect always was significant except for h e glycerol and triglycerides.

Preprandial plasma concentrations of phospholipids and esterified and free cholesterol increased Significantly from wk 3 to 9 (postexperiment) in C but not in 0.

Effects on Jugular-Mammary Differences In Metabolites

In midlactation (trial 2). preprandial differences between J-M vein plasma concentrations (mammary apparent uptake) of triglycerides and esterified cholesterol (Table 2) were higher in 0 than in C. The 0 treatment did not affect mammary apparent uptake of other m e t a b lites.

In early lactation (trial 1), postprandial mammary apparent uptake of triglycerides was higher in 0, whereas preprandial value was not changed; mammary apparent uptake of other metabolites was not affected by 0. Concentra- tion of free glycerol in mammary venous plasma was 19 pill higher (P < .08) than jugular concentration during early lactation (1330 h) and 11 p.M higher (P < .06) during midactation (0830 h) in 0 but not in C treatment.

Significant mammary apparent uptake of plasma phospholipids was observed in the midlactation but not in the early lactation trial, without any significant effect of 0 (C = .ll g/ 1; 0 = .15 g/l; trial 2). No apparent uptake of plasma free cholesterol by the mammary gland was observed in either trial. Preprandial mammary apparent uptake of esterified cholesterol was significant in both trials, and it was significantly increased by 0 in the midlactation trial. Significant mammary apparent uptake of NEFA (about 23% of jugular concentration) was observed in early but not in midlactation.

Data from the two trials were pooled, and the regression slope between J-M differences and jugular concentrations showed that 17% of jugular 3-H33 apparently was taken up by the mammary gland (the intercept of the regression line was not significantly different from zero; Figure 1). For glucose, NEFA, and tri-

J o d of Dairy Science Vol. 74, No. 6, 1991


glycerides (significant intercepts; P e .05), apparent mammary uptake values of 24, 27, and 54% were calculated for jugular concentrations of 70 mg/dl, 1750 pA4, and 300 pM, respectively (Figure 1).

Effects on Plasma Hormones

The scale of blood hormone concentrations was changed by square root transformation prior to ANOVA to equalize variances and to increase accuracy of statistical analysis. In trial 2, lower insulin and higher ST and STinsulin ratio were observed due to 0 in preprandial and postprandial plasma (Table 3). Plasma IGF-I and T3 levels were not affected significantly by 0.

In early lactation (trial 1). plasma levels of insulin, ST, and T3 and the STinsulin ratio were not affected by 0. Using the calculated energy balance (13) as covariate, a lower preprandial plasma insulin level was observed, however, in 0 at wk 1 (C = 14.2 pU/ml, 0 = 11.0 pu/ml, P < .lo).

Changes In Plasma Metabollte Concentmuons after lnsulln Challenge

Decrease in plasma glucose concentration 30 min after a single intravenous insulin injection (Table 4) was not affected by 0 in either early or midlactation trials. These decreases were similar in early (-21 mg/dl) and midlactation (-22 mg/dl). In midlactation (trial 2), plasma glucose concentration 120 min after insulin challenge was lower than preinjection concentration in C but not in 0 cows, and a significant between-group difference was observed. There were no differences between treatments in plasma insulin levels 30 min after insulin challenge in either early or midlactation. Plasma insulin concentration 120 min after insulin injection was higher in C cows during the midlactation trial. Decreases in plasma NEFA concentration 30 min after insulin injection were not affected by 0 in either trial; they were much greater in the early (-160 to -200 CrM) than in the midlactation trial (-20 pM).

DISCUSSION

Effects on Plasma Metabolites

In early (wk 3) and midlactation trials, oiI- free DMI was significantly reduced by 0 (13),

Journal of Dairy Science Vol. 74. No. 6, 1991

potentially decreasing the availability of glucose pmursors, but plasma glucose was not sisnificantly dec~ased. In midlactation, glucose oxidation to yield NADPH probably was lowered as indicated by lowered adipose and mammary de novo lipogenesis (7). A probable enhanced hepatic gluconeogenesis and lowered utilization of gluconeogenic amino acids, linked to a d e c r d mammary protein secretion (13), also may have contributed to main- taining glycemia in 0 cows. Abomasal infusion of safflower oil (28) and soy lecithin (17) reduced DMI but not plasma glucose in midlactation cows. In early lactation, reductions in DMI without changes in plasma glucose were observed with protected tallow (5, 33).

Plasma NEFA often are increased by vegetable oils given in protected form (15) or infused into the abomasum (28) as well as by protected tallow (5, 33) and crystalline fat (6, 29). In midlactation, the higher triglyceride uptake in mammary (Table 2) and adipose tissues (7) in 0 cows may have contributed to the increase in plasma NEFA, because some NEFA may be released into the blood during triglyceride hydrolysis by tissue lipoprotein lipases, but this hypothesis was not confirmed by J-M differences. Higher plasma NEFA levels also were consistent with enhanced adipose tissue lipolytic activities in vitro and with the in vivo response to the beta-agonist isoproterenol in 0 cows (14).

In early lactation, a higher calculated energy balance was observed in 0 due to the lower milk potential and yield of cows (13). This higher energy balance rather than 0 probably accounted for the slightly lower blood NEFA in 0 cows. Feeding fat to lactating ruminants is not

ketogenic, because fatty acids ace absorbed as triglycerides in chylomicrons and very low density lipoproteins and mostly diverted away from the liver toward the extrahepatic tissues (8). Oil fatty acids in either trial led to increases in plasma 3-HB concentration, even when plasma NEFA were increased in midlactation. Nonesterified fatty acids and 3-HB were not correlated in either trial. This lack of com- lation, in spite of increased NEPA and possi- bly gluconeogenesis, could be related to the

ing the entry rate of exogenous 3-KB arising from rumen butyrate. No effects on plasma

Observed d-ws in oil-& DMI (13) limit-

HORMONES AND METABOLJTES IN OIIrINpuSED COWS 1897

TABLE 1. Effect of rapeseed oil infusion on plasma metabolita in early (trial 1) and midlactation (eial 2). ~

Trial 1 Trial 2 0830 h' 0830 h 1330 h

1330 h. W k 17 Wk 17 Wk-1 W k l W k 2 W k 3 Wkg2 w k 2 to 26 to 26

Glucose mg/dl c3 57

SD4 7 0 53

3-HB, Wf C 640 0 760 SD 250

C Wf 810 0 920 SD 360

C 23 0 23 SD 11

C 280 0 244 SD 69

C .83 0 1.11 SD .2 1

cholesterol, C .74 0 .79 SD .2 1

C .15 0 .19

Free glycerol, Wf

Triglycerides, p M

phospholipids, gjL

Esterified

Free cholesterol, @

54 55t 58 68' 47 46 53 66c 10 7 8 5

1340 830 650 35od 1010 960 900 4 5 6 460 360 370 110

1710 1420t 810 49od 1280 1040 750 476 450 380 260 310

55 44 41 49 37 45 43 42 27 18 19 31

165 163 166 193 187 166 185 180 42 3 0 4 0 53

.83 .91 1.26 1.72e 1.09t 1.14 1.75, 1.57 .22 98 .35 .32

.63 .67 .78 1.13e

.82 .88 .97 .99 21 22 .22 .I7

.15 .15 .25 .32d 9ot 20 .30 29

SD .03 .04 .05 .06 .06

48b 45 6

1040 1090 420

630b

240

50 3 1" 25

135b 159b 35

530b

.99b l.2Sb .32

.71a

.88

.25

.16'

.20

.Mi

65 61

5

288 398 161

1% 288 140

28 20 11

1% 2 m * 31

1.90 2.55**

.39

1 .a 2.02** .33

.32

.a**

.08

55 54

5

1572 1525 690

71 114** 20

28 28 11

168 210** 30

1.86 2.63**

.31

1.45 2.08** .a

.32

.4**

.06

%iffemt from 0830 h value in the same treatment at wk 2 (P < .10 and P < .01, respectively). c.4%ifferent from wk 3 in the same group of cows (P < .lo, P < .05, and P < .01, respectively). 'Before (0830 h) or 4.5 h (1330 h) aftex feading. ~ A U cows on mntml diet @osttreabncnt va~ues). 3C = Confrok 0 = rapeseed oil W o n (1.0 to 1.1 kgd); 3-HE = Ihydroxybatyrate. 4 ~ ~ 1 4 SD from within treatment tP < .IO. *P i .05. **P < .01.

ketones were reported with abom sa l oil infusion (17, 28) or by feeding protected oil (16). Protected tallow has been shown to decrease concentrations of plasma ketones in early lactation (5, 21).

Plasm ~ glycerol COD entrati n in the early lactation t& did not reflect the more negative energy balance of C cows (13). probably as the result of a partial hydrolysis of adipose tissue triglycerides (14), or a high plasma glycerol

Joomal of Dairy Science Vol. 74, No. 6, 1991

1898 GAGLIOSTRO ET AI..

TABLE 2. Effect of rapeseed oil infasion on differences between jugular and mammary vein plasma metabolites in early (trial 1) and midlactation (crial 2).

Trial 2, 0830 h 1330 h 0830 h

Trial l1

Glocose. mg/dl C* 1 1' sc 14' 0 ac sc 1 8 SD3 4 4 5

3-HB. w C 0 SD

C 0 SD

W A , W

Triglycerides, pM C 0 SD

Esterified cholesterol, gfL C 0 SD

1 7 6 130 19@ 2 3 6 80 160

320b 13ObVd

210 130 310b 160b

24 31" 35

9oC 1 1 6 60

10 10

100

.05b .08

.06b .02

.04 .10

%b*%erent from 0 (P < .lo, P < .OS, and P < .01, respectively). d,e.fDifferent from 0830 h value (P < .lo, P < .05, and P < .01, respectively). 'Second week of lactation. ' C = Control; o = rapes& oil infusion (1.0 to 1.1 3 ~ 0 0 ~ SD from within treatment. **Significant treatment effect (P < .01).

turnover rate, or both. This result does not confirm the observation (21) that protected tallow lowered plasma glycerol in lactating

Increases in concentrations of all plasma lipids by feeding unprotected or protected lipids have been reported consistently as the consequence of increases in all plasma lipoprotein fractions (8). Higher plasma levels of cholesterol, phospholipids, and triglycerides in the cows of the midlactation trial agree with the general trend. The possible exception to plasma lipid increase after fat feeding are triglycerides, owing to their rapid turnover (8). which may explain the lack of effect of 0 on plasma triglycerides in the early lactation trial. In this trial, plasma phospholipids and free and esterified cholesterol did not increase significantly from wk 3 to 9 when 0 was stopped in the 0 group, contrary to what happened in the C group (Table 1). The lack of increase in the

cows.

0 group at this time probably resulted from elevated plasma concentrations induced by 0 at wk 3 that were not significant in between- group comparisons due to the smal l number of cows and individual variability.

Effect on Jugular-Mammary Differences In Metabolites

Our failure to find a rapeseed oil effect on mammary apparent uptake of glucose (Table 2) is in accordance with data obtained with protected safflower oil (16) and when the oil was infused into the abomasum at a rate of 250 ml/ d (28). Uptake was decreased at a higher infusion rate (500 d d ) without apparent explana- tion (28). The equation in Figure 1 shows a mammary apparent uptake of up to 24% when jugular glucose concentration increased to 70 mg/dl; the considerable scatter observed here and by others (1, 30) is in keeping with the


HORMONES AND METABOLITES IN OIL-INFUSED COWS

500-

400 -

300-

200 -

loo' -

1899

Y = 30 + .17 X (r2= S4))

I

I

I I

I

D

% # A

A I"

0 II I

I

t P o 0 T . l r n 1 1 . 1

1 Y = -60 + .30 X (r2 = .65)

25-

20 - h

3 M s i2 Q 2 10-

15 -

z CI

5 -

0 -

r

200' Y = -80 + .81 X (r2= .69) A

A k A A A

Y = -8.9 + .37 X (r2 = .46)

i B A A A I

I t

A

t I t

I + 100 -

t A A n l n I 8 + e 2 D%# 'u t t 2

1 1 1 +zi t

I Dm I r 8 , I c: 0 - I AD

0 I D I

I D I

A I

I 1 I . I -100 -t ' ' I 1 . 1

400 1 D I

D

I

I n

I

D

-2004 - I

~

I 1 . 1

0 500 loo0 1500 2000

E s

z

Figure 1. Relationships between jugular-mammary (J-M) difference Cy) and jugular concentration (rS, of plasma metabolites (3-HB = 3-hydrOxybntyrate) in early and midlactation (mid) COWS (C = controls; 0 = oil-infused, n = 42). C early = 0 0 early = H; C mid = +; 0 mid = A.

observation that factors other than plasma glucose concentration determine mammary glucose uptake (1).

The higher mammary apparent uptake of triglycerides in the 0 cows of the midlactation trial was consistent with the increase in this plasma metabolite because jugular concentration and apparent uptake were linked closely (r2 = .69, P e .Ol), and it can be calculated that 1 to 54% apparently was taken up by the

mammary gland in the 100 to 300 range of juguIar concentration (Figure 1). A similar r e lationship was reported for an equivalent plasma triglyceride range (80 to 320 pM), and, at higher concentrations, a fall in mammary uptake may be expected (1). In midlactation, a high efficiency of uptake of hydrolyzed fatty acids can be hypothetised, because J-M differences of NEFA were slightly positive (Table 2) despite the simultaneous release of free fatty

Journal of Dairy Science Vol. 74. No. 6. 1991


TABLE 3. Effect of rapeseed oil infusion on plasma hormones in early (trial 1) and midlactation (trial 2).'

Trial1 Trial 2 0830 h 0830 h 1330 h

1330 b, wk 17 wk 17 wk-1 w k l w k 2 w k 3 w k 9 w k 2 to 26 to 26

112 13.4 13.0 20.4 21.3 17.3 15.8* 31.9t Ins* pum

0 15.1 12.0 11.1 15.3 19.0 19.6 13.2 23.6 SD4 5.7 2.9 1.6 7.9 7.0 8.9 3.7 11.4

c3

ST, nghnl C 6.5 7.3 5.1 7 2 4.4 9.8' 2.5 2.0 0 8.6 7.5 7.2 4.8 3.5 11.1 4.6* 2.77 SD 5.5 4.3 3.3 3.3 8.7 5.6 2.1 1.1

C .72 .62 .41 .42 .57 .60 .19 .07 0 .59 .65 .63 .34 21 .76 .41** .15* SD .54 .44 .27 .27 .39 50 29 .OS

C ND5 ND ND ND ND ND 187 149 0 ND ND ND ND ND ND 163 160 SD 70 76

STinsulin ratio

IGF-I. U@

T3, C 1.4 1.2 1.1 1.1 1.4 1 .7b 1.3 1.8 0 1.6 9 1 .o 1 .o 1.2 1.3= 1.4 1.9 SD .5 .4 .2 .2 .5 .5 .3 .3

a, bDifferent from 0830 h value in the same trealment at wk 2 (P < .Os; P < .01, respectively). 'Square mot tranSformation of data was a~ed prior to analysis of variance. 'AU cows on control diet @sttreatment values). 3C = Control; 0 = rapseed oil infusion (1.0 to 1.1 kg/d); ST = somatotmphx IGF-I = insulin-like growth-factor-I; T3

triiodothyronine. POO OM SD from within m n t .

t P < .lo. 5ND = Not determined.

*P < .os. **P < -01.

acids during triglyceride hydrolysis, For glycerol, the other end product of triglyceride hydrolysis, significant negative J-M differences were observed in early (-19 pM; 1330 h) and midlactation (-11 pM) in 0 but not in C, probably indicating mammary release of ex- cess glycerol when triglyceride fatty acid uptake was enhanced.

The higher postprandial mammary apparent uptake of triglycerides observed in 0 in early lactation (Table 2) cannot be attributed to higher metabolite concentration (Table 1). A higher activity of lipoprotein lipase may have been involved due to increased sensitivity to lipolysis of low density lipoprotein triglycer-

ides rich in linoleic acid (16) or lipoproteins rich in unsaturated phospholipids (17). Lower preprandial than postprandial mammary apparent uptake of triglycerides in both groups p a - ble 2; trial l) could be related to a probable inhibition of mammary lipoprotein lipase by the high plasma NEFA concentration (24).

The positive effect of 0 on mammary apparent uptake of triglycerides in both trials was in accordance with results of Gooden and Lascelles (16) but not with those of Rindsig and Schultz (28). Changes in milk fatty acid composition (7) also were consistent with the higher mammary apparent uptake of triglycerides in 0 groups.


HORMONES AND METABOLTTES IN OLINFUSED COWS 1901

TABLE 4. changes in jugular metabolites after insulin challenge (.12 U/kg B'W) in early (trial 1) and midlactation (trial 2).

Trial 11 Trial2 dz 0 sd C 0 SD

PUW 17 20 9 28 27 15 1304 185 175 29 134 171 74 11204 ND6 ND 44t 2s 20

-21C -2 1c 6 -22c -2ZC 9 I126 ND ND -9 -3* 11 I 3 6

11205 ND ND +10 +20 40

Glucose? @dl 48 45 6 57 52 6

m A 3 w 630 530 240 70 120* 30 1305 -2oob -1aOb 150 -20 -20. 30

qb*Qifferent from o (P < .IQ P < .OS; P < .01, rtspactively). lpyk 2 of lactation. %2 = Cone04 0 = rapeseed oil infusion (1.0 to 1.1 kg/d); SD = pooled SD from within treatment.

3~einjection concentrations. 4C0ncentrati0ns 30 or 120 min after insulin injection. '~ecna4e (-1 or increase (+) in concentration 30 (1301 or 120 (1120) min afta iosnlin injection wit^^ respect to

preinjection concentrations. 6ND = Not determined. tP < .lo. *P < .os.

Elevated plasma NEFA levels in the early lactation trial (Table 1) resulted in significant amounts apparently being taken up by the mammary gland (Table 2). Pooled data in Fig- ure 1 confirm that 0 to 27% of jugular plasma NEFA (200 to 1750 pA4 range) may be taken up according to their blood concentration (9 = .65, P < .01), as was previously observed when plasma NEFA concentration was higher than

The lack of rapeseed oil effect on J-M differences in 3-HB is consistent with the similar concentrations of 3-HB in jugular plasma between treatments, because both parameters were linked (r2 = .54, P < .01; Figure 1). A linear relationship has been observed by others over the same range of concentrations (up to 2 mM) with an apparent uptake higher (slope = .41) (30) or similar (slope = .20) (1) to the .17 observed here (Figure 1).

Although composition of jugular blood does not exactly reflect arterial blood composition, the good accordance with literature &ta based on mammary arteriovenous differences sug-

250 pq/L (20).

gests that J-M differences can be used to evaluate general trends.

Effect on Plasma Hormones

A shortage of glucose precursors in the present midlactation trial (13) may have been involved in the slight decrease in plasma insulin in 0. The substitution of whole cottonseed for grain starch also was followed by lower plasma glucose and insulin (1 8). A decrease in plasma glucose and insulin with a r e d u d DMI has been observed in lactating cows fed a protected lipid supplement (27). Lower plasma insulin with similar plasma glucose in midlactation cows fed whole cottonseed was attributed to a less positive energy balance (12). In our experiment, estimated energy balance probably was not involved, because it was higher in 0 cows (13). Neither insulin nor glucose was affected by fat feeding in other trials (6, 22, 29), although energy balance (6, 29) or energy intake (22) was higher in supple- mented cows.

In the present midlactation trial, oil lipid infusion decreased milk protein percentage and yield (13). Palmquist and Moser (27) postu-



lated mediation by insulin resistance, as evi- denced by impaired glucose clearance and enhanced insulin secretion in response to glucose injection in cows fed fat. An increased peak of plasma glucose concentration following glucose challenge was observed in lactating dairy cows fed whole cottonseed (12). Whether the higher plasma glucose recovery 120 min after insulin challenge in 0 cows reflected insulin resistance is uncertain because it was coupled with lower plasma insulin concentration (Table 4).

Glucose decreases 30 min after insulin injection were similar in early and midlactation trials, although insulin resistance often is postulated in early lactation (34). However, a tendency for a lower hypoglycemic response at wk 2 than at wk 7 of lactation was observed in a similar trial (4).

The decrease in plasma NEFA after insulin challenge was not affected by 0 in either trial (Table 4). This decrease was very high in early lactation (about 30%) in accordance with Ber- nal-Santos (4), who observed a 25 to 30% decrease 20 min after injection of .25 insulin units/kg BW. This fall is well known in ruminants and is related to decreased plasma NEFA entry rates and increased utilization (34). Adipose tissue studies in vitro showed, however, that antilipolytic effects of insulin and glucose were diminished in early lactation at physiological concentrations (23). The decrease in NEFA observed in early lactation was obtained with supraphysiological concentrations of insulin averaging 10 times the preinjection values (Table 4).

Fat feeding during the first 2 to 4 mo of lactation did not seem to affect plasma ST (6, 12, 22, 25, 29), even when DMI was reduced (22) or unaffected (12) and energy intake increased (6, 22, 29) or remained unchanged (12). A decrease in plasma ST during early (32) and the last half of lactation (25) in cows fed fat also was observed. The results of the early lactation trial (Table 2) agreed with the general trend, although those of the midlactation trial did not. In this trial, 0 increased plasma ST in spite of simultaneously increas- ing the energy balance of cows (13). Supple- mental fat also seemed to induce a higher plasma ST:insulin ratio in other trials with lactating cows (2, 26). In growing fattening bulls (19), fat supplementation increased mean ST and peak concentrations but not peak fiequen- CY

Enhanced lipolysis of adipose tissue is associated with a higher plasma STinsulin ratio (34). Our finding of a higher ST:insulin ratio in 0 cows of the midlactation trial is consistent with the higher reduction in empty BW and body condition score (13) and with the higher adipose tissue in vitro lipolytic activities and in vivo NEFA response to isoproterenol (14). These unexpected results (increased body fat mobilization and ST:insulin ratio in spite of increased estimated energy balance) should be confirmed using other fat sources and ways of administration to explain a possible specific effect of duodenal rapeseed oil infusion.

Growth hormone is known to enhance the hepatic production of IGF-I. Plasma IGF-I concentration in early lactation cows was correlated positively with energy balance and neg- atively with plasma ST (29). In spite of its positive effect on plasma ST and energy balance, 0 had no effect on plasma IGF-I in midlactation. In milk-fed calves, infusions of chylomicrons into a mesenteric vein significantly enhanced in vivo hepatic IGF-I production (10). The lack of significant effect in our experiment was consistent with results obtained with fat feeding in lactating cows (29).

In conclusion, 0 did not alter plasma concentrations of glucose, 3-HB, or free glycerol; all plasma Lipid fractions were increased in midlactation, as was mammary apparent uptake of triglycerides in both trials. Oil infusion did not affect plasma hormones in early lactation. It increased ST and decreased insulin in midlactation, where it seemed to have metabolic and endocrine effects that mimicked those of decreased energy balance, even when energy balance was positive and higher than in C.

ACKNOWLEDGMENTS

We thank A. Ollier, E. Girard, and J. N. Rampon for animal care and management and R. Lefaivre, G. Sauvage, and J. Flkhet for laboratory analyses. This work was supported by the Institut National de la Recherche Agronomique “Adipose Tissue” research program. G. Gagliostro was supported by a fel- lowship from the Instituto Nacional de Tec- nologia Agropecuaria (Argentina)-Inter- American Development Bank program.

JoUmat of Dairy Science Vol. 74, No. 6, 1991

HORMONES AND METABOLITES IN OIL-INNSED COWS 1903

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