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The latter half of the 20th century and the early portion of the 21st century will be recognized as the "Golden Age" of lactation biology. This period corresponded with the rise of systemic, metabolomic, molecular, and genomic biology. It includes the discovery of the structure of DNA and ends with the sequencing of the complete genomes of humans and all major domestic animal species including the dairy cow. This included the ability to identify polymorphisms in the nucleic acid sequence, which can be tied to specific differences in cellular, tissue, and animal performance. Before this period, classical work using endocrine ablation and replacement studies identified the mammary gland as an endocrine-dependent organ. In the early 1960s, the development of RIA and radioreceptor assays permitted the study of the relationship between endocrine patterns and mammary function. The ability to measure nucleic acid content of tissues opened the door to study of the factors regulating mammary growth. The development of high-speed centrifugation in the 1960s allowed separation of specific cell organelles and their membranes. The development of transmission and scanning electron microscopy permitted the study of the relationship between structure and function in the mammary secretory cell. The availability of radiolabeled metabolites provided the opportunity to investigate the metabolic pathways and their regulation. The development of concepts regarding the coordination of metabolism to support lactation integrated our understanding of nutrient partitioning and homeostasis. The ability to produce recombinant molecules and organisms permitted enhancement of lactation in farm animal species and the production of milk containing proteins of value to human medicine. These discoveries and others contributed to vastly increased dairy farm productivity in the United States and worldwide. This review will include the discussion of the centers of excellence and scientists who labored in these fields to produce the harvest of knowledge we enjoy today.

The objective of this study was to evaluate the effect of pregnancy, breed, and hair coat on body temperature and sweating rate (SR) of hair sheep. St. Croix White (STX; = 9) and Dorper × STX (DRPX; = 9) ewes (3.6 yr of age) were evaluated over 4 d at 126 d of gestation (PREG) and over 4 d at 46 d postpartum (OPEN) in the shade and sun and in the morning (AM; 0900 to 1200 h) and afternoon (PM; 1300 to 1600 h) after a 20 min acclimation to each condition on each day. Data loggers recorded vaginal temperature (VT) at 10-min intervals for 96 h. Rectal temperature (RT) was measured using a digital veterinary thermometer, and respiration rate (RR) was measured as breaths per minute (bpm). Sweating rate was calculated from measured air properties passing over a shaved (300 cm) and unshaved area of the ewes' body using a portable calorimeter. Data were analyzed using GLM procedures of SAS (SAS Inst. Inc., Cary, NC) with breed, pregnancy status, sun exposure, and time of day as main effects. Mean temperature, relative humidity, temperature-humidity index, wind speed, and solar radiation on the days of data collection were 28.2°C, 82.8%, 80.3, 4.2 km/h, and 237.5 W/m, respectively. There was no difference ( > 0.10) in RT, RR, and SR between DRPX and STX ewes. The PREG ewes had lower RT ( 0.10) in RT. There was no difference in SR ( > 0.10) between the shaved and unshaved area of the ewe. The DRPX ewes had higher ( 0.10). Hair coat did not have an influence on the SR of the ewes, and PREG ewes appeared to use increased respiration as opposed to sweating to help control RT. The narrower range of body temperature, measured as VT, of PREG compared to OPEN ewes may be a protective mechanism for the developing fetus.

The objective of this study was to evaluate the effect of pregnancy, breed, and hair coat on body temperature and sweating rate (SR) of hair sheep. St. Croix White (STX; = 9) and Dorper × STX (DRPX; = 9) ewes (3.6 yr of age) were evaluated over 4 d at 126 d of gestation (PREG) and over 4 d at 46 d postpartum (OPEN) in the shade and sun and in the morning (AM; 0900 to 1200 h) and afternoon (PM; 1300 to 1600 h) after a 20 min acclimation to each condition on each day. Data loggers recorded vaginal temperature (VT) at 10-min intervals for 96 h. Rectal temperature (RT) was measured using a digital veterinary thermometer, and respiration rate (RR) was measured as breaths per minute (bpm). Sweating rate was calculated from measured air properties passing over a shaved (300 cm) and unshaved area of the ewes' body using a portable calorimeter. Data were analyzed using GLM procedures of SAS (SAS Inst. Inc., Cary, NC) with breed, pregnancy status, sun exposure, and time of day as main effects. Mean temperature, relative humidity, temperature-humidity index, wind speed, and solar radiation on the days of data collection were 28.2°C, 82.8%, 80.3, 4.2 km/h, and 237.5 W/m, respectively. There was no difference (0.10) in RT, RR, and SR between DRPX and STX ewes. The PREG ewes had lower RT (0.007) and SR (0.0001) and higher RR (0.007) than OPEN ewes (38.5 ± 0.2 vs. 39.1 ± 0.2°C, 70.2 ± 3.1 vs. 88.3 ± 3.1 g⋅m⋅h, and 79.5 ± 2.2 vs. 72.1 ± 2.2 bpm, respectively). During the PM, RR, RT (0.05), and SR (0.006) were higher than in the AM. In the sun, RR (0.001) and SR (0.0001) were higher than in the shade, but there was no difference (0.10) in RT. There was no difference in SR (0.10) between the shaved and unshaved area of the ewe. The DRPX ewes had higher (0.0001) VT than STX ewes. The PREG ewes had higher (0.001) VT than OPEN ewes during the night time and lower VT than the OPEN ewes during the day time (0.0001). The OPEN ewes had a greater (0.009) daily range of VT than PREG ewes did (2.5 ± 0.4 vs. 1.1 ± 0.4°C, respectively), but there was no breed difference (0.10). Hair coat did not have an influence on the SR of the ewes, and PREG ewes appeared to use increased respiration as opposed to sweating to help control RT. The narrower range of body temperature, measured as VT, of PREG compared to OPEN ewes may be a protective mechanism for the developing fetus.

Mammary epithelial cell (ME C) growth is reduced in continuously milked (CM) mammary glands, and administration of a mammogenic compound such as prostaglandin E 2 (PGE 2 ) at parturition might improve MEC growth in CM tissue. The objectives were to 1) compare MEC turnover, ultrastructure, and gene expression in CM and involuting mammary tissue, and 2) evaluate the effects of CM and intramammary infusion of PGE 2 on early lactation MEC turnover, ultrastructure, mammary gene expression, milk yield, and composition. First- and second-lactation cows (n = 8) were used in a half-udder model, in which one-half was dry for 60 d (CTL) and the other was CM. Udder halves (n = 16) were assigned to a postpartum (PP) treatment of PGE 2 (+PGE 2 ; 875 μg/10 mL of medium-chain triglyceride oil) or no PGE 2 (-PGE 2 ) treatment at parturition and at 72 h PP. Biopsies of CM and CTL quarters were obtained during milk stasis (MS) of the CTL half at 3 and 7 d after dry-off of the CTL half (3d-MS; 7d-MS) and postpartum (PP) at 2 and 4 d (2d-PP; 4d-PP). Milk yield was reduced (P 0.2). Apoptosis was elevated in early lactation regardless of treatment. Ultrastructure was unchanged by dry period length or PGE 2 . In prepartum tissue, involution in CTL halves increased (P 0.1) gene expression. The results confirm that CM reduced milk yield of cows with a mammary growth requirement. Reduced MEC turnover and milk yield were not alleviated by IMI of PGE 2 , which indicates that peripartum PGE 2 concentrations in CM glands are not limiting mammary growth or milk synthesis.

Selecting domestic animals for tolerance to thermal stress (TS) has been counterproductive, because acclimation involves reducing or diverting metabolizable energy from production to balance heat gain and loss. Ideally, simultaneous selection for increased production and improved thermotolerance is desirable, but to accomplish this at the genomic level the genes associated with acclimation, adaptation, and thermo-tolerance need to be identified. We evaluated the effects of TS on mammary development and gene expression in vitro using a bovine mammary epithelial cell collagen gel culture system. Acute TS was characterized by inhibition and regression of the ductal branches. Gene expression profiling revealed an overall upregulation of genes associated with the stress response and protein repair. In contrast, genes associated with cellular and mammary epithelial cell-specific biosynthesis, metabolism, and morphogenesis were generally downregulated by TS. Future studies will examine the impact of acclimation and adaptation on gene expression to identify those genes associated with acquisition of thermal tolerance.

The 20 yr of commercial use of recom- binant bovine somatotropin (rbST) in the United States provide the backdrop for reviewing the outcome of use on human health issues by the upcoming 78th meet- ing of the Joint Food and Agriculture Organization of the United Nations (FAO)/World Health Organization (WHO) Expert Committee on Food Additives. These results and further advancements in scientific knowl- edge indicate there are no new human health issues related to the use of rbST by the dairy industry. Use of rbST has no effect on the micro- and macrocompo- sition of milk. Also, no evidence exists that rbST use has increased human exposure to antibiotic residues in milk. Concerns that IGF-I present in milk could have biological effects on humans have been allayed by stud- ies showing that oral consumption of IGF-I by humans has little or no biological activity. Additionally, con- centrations of IGF-I in digestive tract fluids of humans far exceed any IGF-I consumed when drinking milk. Furthermore, chronic supplementation of cows with rbST does not increase concentrations of milk IGF-I outside the range typically observed for effects of farm, parity, or stage of lactation. Use of rbST has not affected expression of retroviruses in cattle or posed an increased risk to human health from retroviruses in cattle. Furthermore, risk for development of type 1 or type 2 diabetes has not increased in children or adults consuming milk and dairy products from rbST-supple- mented cows. Overall, milk and dairy products provide essential nutrients and related benefits in health mainte- nance and the prevention of chronic diseases.

Bovine placental lactogen (PL) is a partial somatotropin agonist in the cow and decreases urea nitrogen, indicating increased nitrogen retention. In the present study, the somatogenic effects of bovine PL (bPL; 4 and 8 mg/d) were compared with those of bovine somatotropin (bST; 4 and 8 mg/d) in finishing lambs. Measures of comparison included growth per- formance, carcass composition, and growth-related clinical chemistry traits. Although feed efficiency during the first 3 wk of treatment with bPL was improved by 14% (P < .05), feed efficiency for the full 6-wk treatment period did not differ from that of control lambs. Responsiveness to bPL may have been attenuated by high titer antibodies present after 2 wk of treatment. However, bPL also did not influence growth-related clinical chemistry traits during short- term (7 d) treatment, strongly suggesting that bPL was ineffective in finishing lambs at the doses tested. In contrast, bST improved 6-wk feed efficiency by an average of 17% (P < .05) and decreased feed intake by an average of 12% (P < .05). In addition, measures of carcass composition including longissimus muscle area, specific gravity of the rack, kidney and pelvic fat, and fat thickness demonstrated that bST, but not bPL, treatment decreased carcass fatness and increased carcass leanness. Treatment with bST, but not with bPL, affected IGF-I, insulin, glucose, and urea nitro- gen in a dose-related manner. Thus, daily injections of bPL did not affect either performance or carcass quality, whereas performance and carcass responses of finishing lambs to bST were consistent with those reported by others.

Eighteen Chianina crossbred steers were used to examine the interrelationship between hormonal status and empty body protein (EBPRT) and fat (EBFAT) accretion during an 88-d controlled realimentation (REAL; DMI was adjusted weekly on an individual BW basis) period. Body composition was determined by monitoring endogenous whole-body 40[K]. At the end of restriction (REST) and on d 31 and 59 of REAL blood samples were taken and analyzed for concentrations of growth hormone (GH), IGF-I, IGF-II, insulin (INS), thyroxine (T4), triiodothyronine (T3), reverse triiodothyronine (rT3), nonesterified fatty acids (NEFA), glucose, and urea nitrogen. Depositions of EBPRT and EBFAT were decreased (P < .001) in REST (92 d) animals compared with nonrestricted (NR) controls. During REST, plasma levels of glucose, IGF-I, INS, T4, T3, and rT3 were decreased (P < .05); plasma urea nitrogen (PUN), NEFA, and GH levels were increased (P < .05), and IGF-II concentrations were similar between REST and NR steers. A transient compensatory response in BW gain and protein deposition occurred in repleted steers between d 35 and 62 of REAL. During this period, PUN levels markedly declined (P < .01) in REAL steers and glucose concentration increased (P < .01) to levels similar to those in NR controls. This response prevailed even though apparent digestible nutrients were decreased in repleted animals. During energy repletion, plasma levels of T4, T3, rT3, IGF-I, and INS were positively, and of GH was negatively, correlated with EBPRT and EBFAT gain in repleted animals. Unlike IGF-I, IGF-II was not correlated with compensatory body growth. These results suggest that compensating steers are more metabolically efficient; rapid body tissue gain occurs during a period of reduced nutrient digestibility. Additionally, plasma levels of IGF-I, GH, INS, and thyroid hormones, but not of IGF-II, are markedly affected by alteration of energy intake and are highly correlated with empty body gain and protein deposition in compensating late-maturing steers.

Ruminant placental lactogens (PL) are members of the somatotropin, prolactin gene family that are synthesized by trophectodermal binucleate cells. The structure and biology of PL has been studied in the cow, sheep, and goat. Ruminant PL have greater structural identity to prolactin than somatotropin, although they bind to both lactogenic and somatogenic receptors. The molecular weights of ovine and caprine PL are approximately 23,000, whereas bovine PL is larger (31,000 to 34,000) due to glycosylation. Placental lactogen is secreted into both the fetal and maternal circulations. The concentration of PL in the fetus decreases with advancing gestation, whereas PL concentration peaks in the maternal circulation during the last third of pregnancy then reaches a plateau. Furthermore, the maternal concentration of PL is 100- to 1,000-fold higher in sheep and goats than in cows. The precise factors that modulate secretion of PL are unknown, although placental mass and nutrition seem to play a role. Ruminant PL have both lactogenic and somatogenic biological activities and may also have unique activities mediated through a specific receptor. There is circumstantial evidence to suggest that PL plays a role in stimulating mammogenesis. Placental lactogen secreted into the fetal compartment may also help regulate fetal growth. Direct experimental data indicate that PL can regulate maternal intermediary metabolism. Thus, it may act as a partitioning agent to regulate nutrient supply for fetal growth. The precise biological function of PL in ruminants, therefore, still needs to be defined.

A series of studies examined the binding characteristics and ontogeny of hepatic growth hormone binding sites in dairy bulls on d 2, 30, 180, and 365 of age. Binding of iodinated recombinant bovine growth hormone ([125I]rbGH) to liver membrane receptors was membrane protein-dependent. Receptors were considered growth hormone-specific, because physiological concentrations of bovine prolactin (bPRL) failed to displace [125I]rbGH from bovine hepatocyte membranes. Only 50% of [125I]rbGH was bound reversibly to hepatic microsomes. Addition of dithiothreitol (DTT) to the receptor-assay buffer increased the binding of [125I]rbGH to hepatic membranes in a time-dependent manner. Moderate concentrations of Ca++ and Mg++ in the receptor-assay buffer had no detectable effects on binding of [125I]rbGH to hepatic microsomes. In growing dairy bulls, specific binding of [125I]rbGH per milligram of membrane protein increased from 1.9 +/- 1.8% at d 2 to 14.1 +/- 1.8% at d 180 and then declined to 5.2 +/- 1.6% at d 365. Likewise, concentration of insulin-like growth factor (IGF)-I in serum was low during the 1st mo of age (d 2, 13.3 +/- 8.8 ng/ml; d 30, 9.7 +/- 8.8 ng/ml), but it became maximal at d 180 (151.0 +/- 8.8 ng/ml). Circulating concentrations of IGF-II increased linearly during the 1st yr of growth. Serum concentrations of GH, triiodothyronine, and thyroxine declined from 39.9 +/- 6.5, 2.7 +/- .2, and 75.4 +/- 4.6 ng/ml at d 2 to 16.5 +/- 6.5, 1.3 +/- .2, and 53.4 +/- 4.6 ng/ml at d 30, respectively, and remained low through 1 yr of age. Insulin concentration in serum did not change significantly with development. Results indicated that increasing concentrations of specific bGH receptors in the bovine liver may play a key role in regulating postnatal growth in cattle.

Our objective was to evaluate effects of acute thermal stress, independent of reduced feed intake caused by elevated temperatures, and of reduced feed intake in thermal comfort on plasma concentrations of somatotropin, insulin-like growth factors I and II, thyroxine, and triiodothyronine. Six Holstein cows (averaging 475 +/- 18 kg BW, 2.3 +/- .3 parities, and 96 +/- 12 d in lactation) surgically fitted with catheters in the hepatic portal vein, mesenteric vein, and intercostalis posterior artery were exposed to treatments of thermal comfort environments with ad libitum or restricted (75% of ad libitum) DM intake and a thermal stress environment with ad libitum intake in two balanced 3 x 3 Latin squares. Thermal stress increased rectal temperatures and respiration rates. Dry matter intake of the thermal-stressed cows offered feed ad libitum (11.1 +/- .7 kg/d) was similar to the experimentally imposed reduction in DM intake of the thermal comfort restricted group (11.5 +/- .7 kg/d). Dry matter intake of cows in thermal comfort was 15.1 +/- .7 kg/d. Plasma somatotropin concentrations tended (P less than .08) to decrease during thermal stress but were unchanged by amount of feed intake in thermal comfort environments. Concentrations of IGF-I were not affected by treatments. Concentrations of IGF-II tended (P less than .14) to increase with thermal stress compared with thermal comfort treatments. Thyroxine concentrations tended (P less than .15) to increase in the thermal stress treatment compared with the thermal comfort restricted intake treatment. Triiodothyronine tended (P less than .11) to decrease with restriction in feed intake in the thermal comfort environment.(ABSTRACT TRUNCATED AT 250 WORDS)

Mammary epithelial cell (MEC) growth is reduced in continuously milked (CM) mammary glands, and administration of a mammogenic compound such as prostaglandin E(2) (PGE(2)) at parturition might improve MEC growth in CM tissue. The objectives were to 1) compare MEC turnover, ultrastructure, and gene expression in CM and involuting mammary tissue, and 2) evaluate the effects of CM and intramammary infusion of PGE(2) on early lactation MEC turnover, ultrastructure, mammary gene expression, milk yield, and composition. First- and second-lactation cows (n = 8) were used in a half-udder model, in which one-half was dry for 60 d (CTL) and the other was CM. Udder halves (n = 16) were assigned to a postpartum (PP) treatment of PGE(2) (+PGE(2); 875 mug/10 mL of medium-chain triglyceride oil) or no PGE(2) (-PGE(2)) treatment at parturition and at 72 h PP. Biopsies of CM and CTL quarters were obtained during milk stasis (MS) of the CTL half at 3 and 7 d after dry-off of the CTL half (3d-MS; 7d-MS) and postpartum (PP) at 2 and 4 d (2d-PP; 4d-PP). Milk yield was reduced (P0.01) in CM udder halves compared with CTL halves (13.2 vs. 22.1 kg/d), but reductions were less in second-lactation cows. The apoptotic index was greater (P0.05) in CTL glands than in CM glands (3d-MS, 0.52 vs. 0.11% and 7d-MS, 0.24 vs. 0.12, respectively). Proliferation of MEC was unchanged at 3d-MS, but was increased (P = 0.01) in CTL halves at 7d-MS compared with CM halves (3.10 vs. 0.93%). At 2d-PP, MEC proliferation was increased (P = 0.05) in CM halves compared with CTL halves (1.3 vs. 0.6%), but was unaffected by PGE(2) (P0.2). Apoptosis was elevated in early lactation regardless of treatment. Ultrastructure was unchanged by dry period length or PGE(2). In prepartum tissue, involution in CTL halves increased (P0.05) the expression of the proapoptotic genes Bcl-2-associated x protein (bax) and IGFBP5 and decreased (P0.05) alpha-lactalbumin expression compared with CM tissue. In PP mammary tissue, CTL halves expressed greater (P0.05) levels of ATP-binding cassette 1 (ABC1) and IGFBP5. Treatment with PGE(2) did not alter (P0.1) gene expression. The results confirm that CM reduced milk yield of cows with a mammary growth requirement. Reduced MEC turnover and milk yield were not alleviated by IMI of PGE(2), which indicates that peripartum PGE(2) concentrations in CM glands are not limiting mammary growth or milk synthesis.

Selecting domestic animals for tolerance to thermal stress (TS) has been counterproductive, because acclimation involves reducing or diverting metabolizable energy from production to balance heat gain and loss. Ideally, simultaneous selection for increased production and improved thermotolerance is desirable, but to accomplish this at the genomic level the genes associated with acclimation, adaptation, and thermo-tolerance need to be identified. We evaluated the effects of TS on mammary development and gene expression in vitro using a bovine mammary epithelial cell collagen gel culture system. Acute TS was characterized by inhibition and regression of the ductal branches. Gene expression profiling revealed an overall upregulation of genes associated with the stress response and protein repair. In contrast, genes associated with cellular and mammary epithelial cell-specific biosynthesis, metabolism, and morphogenesis were generally downregulated by TS. Future studies will examine the impact of acclimation and adaptation on gene expression to identify those genes associated with acquisition of thermal tolerance.

Our objective was to evaluate effects of acute thermal stress, independent of reduced feed intake caused by elevated temperatures, and of reduced feed intake in thermal comfort on plasma concentrations of somatotropin, insulin-like growth factors I and II, thyroxine, and triiodothyronine. Six Holstein cows (averaging 475 +/- 18 kg BW, 2.3 +/- .3 parities, and 96 +/- 12 d in lactation) surgically fitted with catheters in the hepatic portal vein, mesenteric vein, and intercostalis posterior artery were exposed to treatments of thermal comfort environments with ad libitum or restricted (75% of ad libitum) DM intake and a thermal stress environment with ad libitum intake in two balanced 3 x 3 Latin squares. Thermal stress increased rectal temperatures and respiration rates. Dry matter intake of the thermal-stressed cows offered feed ad libitum (11.1 +/- .7 kg/d) was similar to the experimentally imposed reduction in DM intake of the thermal comfort restricted group (11.5 +/- .7 kg/d). Dry matter intake of cows in thermal comfort was 15.1 +/- .7 kg/d. Plasma somatotropin concentrations tended (P less than .08) to decrease during thermal stress but were unchanged by amount of feed intake in thermal comfort environments. Concentrations of IGF-I were not affected by treatments. Concentrations of IGF-II tended (P less than .14) to increase with thermal stress compared with thermal comfort treatments. Thyroxine concentrations tended (P less than .15) to increase in the thermal stress treatment compared with the thermal comfort restricted intake treatment. Triiodothyronine tended (P less than .11) to decrease with restriction in feed intake in the thermal comfort environment.(ABSTRACT TRUNCATED AT 250 WORDS)

A series of studies examined the binding characteristics and ontogeny of hepatic growth hormone binding sites in dairy bulls on d 2, 30, 180, and 365 of age. Binding of iodinated recombinant bovine growth hormone ([125I]rbGH) to liver membrane receptors was membrane protein-dependent. Receptors were considered growth hormone-specific, because physiological concentrations of bovine prolactin (bPRL) failed to displace [125I]rbGH from bovine hepatocyte membranes. Only 50% of [125I]rbGH was bound reversibly to hepatic microsomes. Addition of dithiothreitol (DTT) to the receptor-assay buffer increased the binding of [125I]rbGH to hepatic membranes in a time-dependent manner. Moderate concentrations of Ca++ and Mg++ in the receptor-assay buffer had no detectable effects on binding of [125I]rbGH to hepatic microsomes. In growing dairy bulls, specific binding of [125I]rbGH per milligram of membrane protein increased from 1.9 +/- 1.8% at d 2 to 14.1 +/- 1.8% at d 180 and then declined to 5.2 +/- 1.6% at d 365. Likewise, concentration of insulin-like growth factor (IGF)-I in serum was low during the 1st mo of age (d 2, 13.3 +/- 8.8 ng/ml; d 30, 9.7 +/- 8.8 ng/ml), but it became maximal at d 180 (151.0 +/- 8.8 ng/ml). Circulating concentrations of IGF-II increased linearly during the 1st yr of growth. Serum concentrations of GH, triiodothyronine, and thyroxine declined from 39.9 +/- 6.5, 2.7 +/- .2, and 75.4 +/- 4.6 ng/ml at d 2 to 16.5 +/- 6.5, 1.3 +/- .2, and 53.4 +/- 4.6 ng/ml at d 30, respectively, and remained low through 1 yr of age. Insulin concentration in serum did not change significantly with development. Results indicated that increasing concentrations of specific bGH receptors in the bovine liver may play a key role in regulating postnatal growth in cattle.

Effects of fetal sire on postpartum reproductive changes of the dam were studied in 21 Holstein heifers whose pregnancy had been initiated by either Angus (n = 7), Holstein (n = 7) or Brahman (n = 7) bulls. After parturition, all heifers were managed uniformly. Heifers in each service-sire-breed group were bled via jugular venipuncture thrice weekly from d 160 to 265 of pregnancy, daily thereafter until 15 d postpartum, and three times per week until d 60 postpartum. Ability of heifers to release prolactin (PRL) and luteinizing hormone (LH) was evaluated on d 10 postpartum after a simultaneous injection of thyrotropin releasing hormone (TRH; 100 micrograms) and gonadotropin releasing hormone (GnRH; 100 micrograms). Between d 5 and 60 postpartum, the reproductive tract of each heifer was examined rectally thrice weekly after collection of blood samples. Basal concentrations of LH from d 1 to 10 postpartum, as well as ability of the pituitary gland to release LH and PRL after the GnRH-TRH challenge, did not differ between service-sire-breed groups (P greater than .1). Means and profiles of progesterone concentrations during the first 60 d postpartum did not differ between service-sire-breed groups (P greater than .1). However, increases in progesterone concentrations following the GnRH-TRH challenge were synchronized more precisely in Angus (P less than .02) than in Holstein- and Brahman-service-sire groups. Daily rates of reduction in cervical and uterine horn diameters were higher (P less than .01) in Holstein- and Brahman- than in Angus-service-sire groups and were associated with higher profiles of postpartum 15-keto-13,14-dihydro-prostaglandin F2 alpha (PGFM) concentrations. Within-cow PGFM concentrations were correlated positively with cervical (r = .36) and uterine horn (r = .32) diameters. Postpartum ovarian responsiveness and uterine involution in Holstein heifers may be affected by genotypes of the conceptus they bore during pregnancy.

Six Holstein cows (averaging 475 kg body weight, 2.3 parities and 96 d in lactation) fitted with catheters in the hepatic portal vein, mesenteric vein and intercostalis posterior artery were exposed to treatments of thermal comfort environments with libitum or restricted (75% of ad libitum) DM intake and a thermal stress environment with ad libitum intake in two balanced 3 x 3 latin squares to evaluate effects of thermal stress on portal plasma flow and net fluxes of metabolites. Portal plasma flow was measured by administering a primed, continuous infusion of para-aminohippurate into a mesenteric vein and determining its concentration and dilution in portal vein plasma. Thermal stress treatment increased rectal temperatures and respiration rates. Dry matter intake decreased from thermal comfort ad libitum level (15.1 kg/d) to lower levels in thermal comfort restricted (11.5 kg/d) and thermal stress (11.1 kg/d) treatments. Portal plasma flow was related directly to level of DM intake, declining about 14% with thermal comfort restricted intake and thermal stress environment treatments compared with the thermal comfort restricted intake and thermal stress environment treatments compared with the thermal comfort ad libitum intake treatment. Net flux of alpha-amino N was reduced 20 and 35% by thermal comfort restricted intake and thermal stress treatments compared with the thermal comfort ad libitum intake treatment. Net fluxes of urea N, ammonia N and glucose were not affected by experimental treatments. A portion of the negative effects of thermal stress on milk production can be explained by decreased nutrient intake and decreased nutrient uptake by the portal-drained viscera of the cow.

Plasma glucose and serum insulin, growth hormone and glucocorticoid concentrations were determined in five yearling bulls given (im) 5, 15 or 30 mg prostaglandin E2 (PGE2), 30 mg prostaglandin F2 alpha(PGF2 alpha) or saline. Jugular blood was collected at frequent intervals around the time of injection and at .5--hr intervals from 1 to 9 hr after injections. Thirty milligrams PGE2 and 30 mg PGF2 alpha each caused 15- to 20-fold increases in serum glucocorticoids. Glucocorticoids increased with increasing doses of PGE2. Although PGE2 and PGF2 alpha each increased blood growth hormone, this effect was about twofold larger after PGE2. By contrast, PGE2 depressed serum insulin about 50% for 1 hr, then insulin increased about sixfold until 3 to 4 hours. Blood serum insulin increased after PGF2 alpha, but this effect only approached significance (P less than .10). Plasma glucose increased about 10 mg/100 ml after PGE2, but was not affected significantly by PGF2 alpha. Thus, the effects of PGE2 and PGF2 alpha on hormones which control glucose metabolism differ markedly. We speculate that PGE2 caused a twofold increase in growth hormone secretion within 10 to 20 min, that increased growth hormone induced increased blood glucose within 1 to 2 hr and that increased glucose caused increased insulin secretion at 2 to 4 hr, but we cannot rule out a transitory (1 hr) suppressive effect of PGE2 directly on the pancreas.

For an evaluation of the effects of heat stress during pregnancy on calf birth weight and postpartum maternal milk yield, 21 cows and 10 heifers were assigned to shade (S; n = 16) or no shade (NS; n = 15) treatments during the last trimester of pregnancy in June 1978. At parturition, all cows were removed from treatment and uniformly managed in the milking herd. At 4-d intervals from d 199 of pregnancy to parturition, respiration rates, rectal temperature, heart rate and Black Globe temperature were recorded and blood samples obtained via tail venipuncture between 1300 and 1600 h. Weekly prepartum body weights of dam, birth weight of calf and subsequent daily milk yield were recorded. Black Globe temperature, rectal temperature and respiration rates were higher in cows given NS. Calf birth weight was lower in the NS group. Milk yield was correlated in a linear manner with calf birth weight, and cows in group NS exhibited reduced lactation performance after calving. Plasma progestin concentrations were higher in heat-stressed cows (6.0 vs 5.1 ng/ml). Estrone-sulfate concentrations were reduced in plasma of NS cows (2,505 vs 4,433 pg/ml). Thus, hormone concentrations of maternal and fetal origin were altered by environment. Plasma thyroxine concentrations were lower in NS cows (51.2 vs 66.4 ng/ml), while plasma triiodothyronine concentrations were elevated (1.8 vs 1.5 ng/ml), indicating altered thyroid hormone metabolism in heat-stressed cows. Heat stress altered endocrine dynamics during pregnancy and reduced calf birth weight and may have indirectly altered subsequent milk yield.

Effects of heat stress during the last third of gestation on reproductive changes postpartum were studied in Holstein cows. Cows and heifers 160 to 190 d of gestation were assigned in June 1978 to shade (n = seven cows and two heifers) or no shade (n = eight cows and two heifers) management treatments. After parturition, all cows (n = 19) were moved to the milking herd and managed uniformly. On the day of calving and on each Monday, Wednesday and Friday thereafter until d 50 postpartum, jugular blood samples were collected. Beginning approximately 7 d postpartum, the reproductive tract of each cow was examined rectally after collection of blood samples. Estrus was monitored twice daily and cows were inseminated after d 45 postpartum. Prepartum heat stress increased 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) concentrations postpartum and increased the rate of uterine involution. Regardless of prepartum treatment, progesterone concentrations indicated that luteal phases had begun by d 12.4 +/- 1.3 postpartum, which was about 3 d before PGFM was basal. The first luteal phase lasted only 10.7 +/- .9 d. First estrus was not detected until d 32.3 +/- 4.8 postpartum. The previously gravid uterine horn had a negative effect on ovarian volume, diameter of the largest follicle and percentage of ovaries with a corpus luteum. However, prepartum heat stress attenuated this effect. This study indicates that heat stress prepartum had residual effects on postpartum reproductive changes, and that the previously gravid uterine horn exerted some control, which was attenuated by heat stress, over ovarian recrudescense. Even though heat stress prepartum affected sensitive measures of postpartum reproductive function, it did not alter days to first estrus, days open (102.3 +/- 13.1) or services/conception (2.5 +/- .3).

Four cows received thyroxine injections (T4; 20 mg/d) and three cows received growth hormone injections (GH, 44 mg/d) for 4 d during successive 16-d experimental periods. Milk fat, lactose output, mammary uptake of glucose, oxygen and milk fat precursors were determined with each treatment. Injection of T4 increased lactose yield by 25% and fat yield 42%. The injection of GH increased fat and lactose yields by 24%. Both GH and T4 increased mammary glucose uptake by 35% and 45%, respectively, while T4 administration was associated with an increase in plasma glucose concentration from 67 to 84%. Thyroxine, but not GH, increased the ratio of mammary glucose uptake to lactose output from 1.24 to 1.58. Blood plasma acetate concentration declined following GH and T4 treatment by 17%. Mammary acetate uptake increased in response to GH injection in two of three cows but did not change with T4 injection. The injection of GH had no effect on plasma propionate concentration or mammary uptake. Thyroxine reduced plasma propionate content and mammary uptake. Neither T4 nor GH changed plasma free fatty acid concentration or mammary uptake. Thyroxine had no effect on plasma triglyceride concentration or mammary uptake, whereas GH increased mammary triglyceride uptake to the end of the experimental period. Mammary oxygen uptake was increased by GH as milk production increased. Increased mammary oxygen uptake following T4 treatment was transient. Change in mammary metabolism with T4 treatment permitted increased milk output without change in mammary oxygen consumption. Such a change may involve increased mammary utilization of pre-formed long-chain fatty acid and increased metabolism of glucose via glycolysis.

Four cows received thyroxine injections (T4; 20 mg/d) and three cows received growth hormone injections (GH; 44 mg/d) for 4 d during successive 16-d experimental periods. Measurement was made of milk yield, protein yield, mammary tyrosine and phenylalanine uptake, blood plasma hormone concentrations, mammary blood flow and cardiac output. Milk yield increased by 25% with T4 and 21% with GH treatment. Milk protein content tended to decline during T4 treatment and increase following GH treatment. Cardiac output increased by 8.9 liter/min (20%) and 4.6 liter/min (10%) with T4 and GH injection. Mammary blood flow (half-udder) increased from 3.6 to 4.9 liter/min (35%) and from 3.3 to 4.4 liter/min (33%) with T4 and GH treatment, respectively. These increases calculated on a whole-udder basis, accounted for 28% (T4) and 48% (GH) of the increases in cardiac output. The proportion of cardiac output perfusing the (whole) udder increased to 19.1% (T4) and 18.7% (GH), increases of 17 and 30%, respectively. Heart rate increased with T4 (but not GH treatment) from 80 to 115/min. Ratio of blood flow to milk yield was not changed by either treatment. The proportion of cardiac output perfusing the udder likely plays a major role in facilitating the partitioning of nutrients for milk synthesis.

Plasma glucose and serum insulin, growth hormone and glucocorticoid concentrations were determined in five yearling bulls given (im) 5, 15 or 30 mg prostaglandin E2 (PGE2), 30 mg prostaglandin F2 alpha(PGF2 alpha) or saline. Jugular blood was collected at frequent intervals around the time of injection and at .5--hr intervals from 1 to 9 hr after injections. Thirty milligrams PGE2 and 30 mg PGF2 alpha each caused 15- to 20-fold increases in serum glucocorticoids. Glucocorticoids increased with increasing doses of PGE2. Although PGE2 and PGF2 alpha each increased blood growth hormone, this effect was about twofold larger after PGE2. By contrast, PGE2 depressed serum insulin about 50% for 1 hr, then insulin increased about sixfold until 3 to 4 hours. Blood serum insulin increased after PGF2 alpha, but this effect only approached significance (P less than .10). Plasma glucose increased about 10 mg/100 ml after PGE2, but was not affected significantly by PGF2 alpha. Thus, the effects of PGE2 and PGF2 alpha on hormones which control glucose metabolism differ markedly. We speculate that PGE2 caused a twofold increase in growth hormone secretion within 10 to 20 min, that increased growth hormone induced increased blood glucose within 1 to 2 hr and that increased glucose caused increased insulin secretion at 2 to 4 hr, but we cannot rule out a transitory (1 hr) suppressive effect of PGE2 directly on the pancreas.

Six Holstein cows (averaging 475 kg body weight, 2.3 parities and 96 d in lactation) fitted with catheters in the hepatic portal vein, mesenteric vein and intercostalis posterior artery were exposed to treatments of thermal comfort environments with libitum or restricted (75% of ad libitum) DM intake and a thermal stress environment with ad libitum intake in two balanced 3 x 3 latin squares to evaluate effects of thermal stress on portal plasma flow and net fluxes of metabolites. Portal plasma flow was measured by administering a primed, continuous infusion of para-aminohippurate into a mesenteric vein and determining its concentration and dilution in portal vein plasma. Thermal stress treatment increased rectal temperatures and respiration rates. Dry matter intake decreased from thermal comfort ad libitum level (15.1 kg/d) to lower levels in thermal comfort restricted (11.5 kg/d) and thermal stress (11.1 kg/d) treatments. Portal plasma flow was related directly to level of DM intake, declining about 14% with thermal comfort restricted intake and thermal stress environment treatments compared with the thermal comfort restricted intake and thermal stress environment treatments compared with the thermal comfort ad libitum intake treatment. Net flux of alpha-amino N was reduced 20 and 35% by thermal comfort restricted intake and thermal stress treatments compared with the thermal comfort ad libitum intake treatment. Net fluxes of urea N, ammonia N and glucose were not affected by experimental treatments. A portion of the negative effects of thermal stress on milk production can be explained by decreased nutrient intake and decreased nutrient uptake by the portal-drained viscera of the cow.

This study examined the effect of number of conceptuses on maternal concentrations and profiles of estrogen sulfate, estrone, estradiol-17 beta, progesterone and prolactin in gilts. Estradiol-valerate injections were used to induce pseudopregnancy (O conceptuses; n = 5) and oviduct ligation or no treatment were utilized to obtain pregnant gilts with 4 to 7 (n = 4), or 8 to 11 (n = 4) conceptuses, respectively. Blood samples were collected every 10 d from d 10 through 110 of pregnancy or pseudopregnancy. At 110 d after onset of estrus, all gilts were slaughtered and numbers and(or) weights of fetuses, corpora lutea, placentae and the empty uterus were determined. Concentrations of estrogen sulfate and estrone, but not progesterone or prolactin, were associated with fetal number, total fetal weight, total placental weight or empty uterine weight. In contrast, only progesterone was highly correlated with number of corpora lutea. Results suggest that most conjugated estrogen, estrone and estradiol were of fetal-placental origin, whereas little, if any, placental production of progesterone or prolactin occurred. Increases in estrogen sulfate and estrone concentrations were observed at gestation d 30 and from d 70 to 100. The latter increase coincides with previously established increases in the rate of maternal mammary development and fetal growth.

Holstein heifers (n = 21) were balanced across sires and assigned to three service-sire-breed groups in which heifers were inseminated artificially to either purebred Angus (n = 7), Holstein (n = 7) or Brahman (n = 7) bulls. Semen from four bulls was used for each service sire-breed group. Blood samples were collected from a jugular vein thrice weekly from d 160 to 265 of pregnancy, daily thereafter until 15 d postpartum, and then thrice weekly until d 60 postpartum. Concentrations of progesterone, estrone, estradiol, and estrone sulfate from 23 d prepartum to parturition, and of 15-keto-13,14-dihydro-prostaglandin F2 alpha (PGFM) from 2 d prepartum to d 15 postpartum were measured by radioimmunoassay. Heifers within the Brahman-service-sire group had longer gestations (P less than .05) than those of Holstein- or Angus-service-sire groups (285.0 vs 278.7), 279.0 d). Calf birth weight was lower (P less than .05) in Angus- than Holstein- and Brahman-service-sire groups (30.6 vs 36.1, 43.4 kg). Daily trends of prepartum maternal progesterone concentrations were approximately 1 ng/ml lower (P less than .01) in Angus- than Holstein- or Brahman-service-sire groups until luteolysis occurred. Heifers bearing crossbred Angus conceptuses had lower daily trends of prepartum estrogens concentrations (P less than .01), whereas heifers of the Holstein- and, even more dramatically, of the Brahman-service-sire groups had a higher magnitude and greater rise of plasma estrogens concentrations between d -10 and -1 prepartum (less than .01). Postpartum mean concentrations (P less than .05) and response curves of PGFM were lower (P less than .01) in the Angus- than in the Holstein- or Brahman-service-sire groups. Calf birth weights were correlated with least-squares means for maternal concentrations of prepartum estrone (r = .57), estradiol (r = .59) and estrone sulfate (r = .64) and postpartum maternal concentrations of PGFM (r = .56). Functional responses of the conceptus (e.g., estrogens) and maternal units (e.g., progesterone and PGFM) were influenced by conceptus genotype during the periparturient period.

Changes in mammary gland histology, dry weights, nucleic acids and in vitro rates of substrate oxidation in incorporation into lipid were measured in mammary biopsies of three gilts each on d 30, 45, 60, 75, 90, 105 and 112 of pregnancy, and d 1 and 4 of lactation. Histological changes noted were progressive duct growth early in pregnancy followed by rapid lobulo-alveolar development between d 75 and 90 to complete mammogenesis. Colostrum and lipid were evident by d 105 with marked distension of alveolar lumina on d 112. Complete differentiation of the secretory process was apparent on the day of parturition. Concentrtion of dry, fat-free tissue (DFFT) and DNA changed little before d 60 but increased fourfold between d 75 and 90. No further increases in DFFT or DNA were noted. RNA concentrations paralleled DNA through d 90, after which they steadily increased. Rates of acetate and glucose oxidation increased transiently during midpregnancy then declined and remained low until initiation of lactogenesis. Substrate incorporation into lipid increased slightly at midpregnancy and again at d 105, after which it increased markedly. Collectively, results indicate that mammogenesis is complete by d 90, after which lactogenesis is initiated in a two-stage process. Metabolic rates expressed on a DNA basis indicated considerable rates of oxidation, but not of lipogenesis by proliferating mammary tissue. Preferential metabolism of acetate vs glucose near parturition suggests coordination of metabolism between the mammary gland and other maternal tissues.

Lactogenesis signals the shift from uterine nutrient transfer to the fetus to neonatal nourishment at the mammary gland. Metabolic adaptations involved in this process are under endocrine regulation. Key events include an increase in blood flow to mammary tissue, a decrease in nutrient utilization by peripheral tissues and an increase in nutrient utilization by mammary tissue for milk synthesis. Deficits of certain substrates during early lactation require mobilization of those substrates from depot stores. Changes in metabolism of various tissues are related to changes in hormone receptor populations of those tissues and hormone concentrations in blood. Hormone receptors are therefore the primary mechanism by which information from the endocrine systems is linked to cellular metabolism. Endocrine changes at parturition result in dramatic changes in receptor populations of key tissues such as adipose and mammary tissues. Knowledge in this area, however, is incomplete. Relationship between hormone receptors and specific cellular metabolic pathways remains unresolved.