Reproduction in Domestic Animals

More documents

Recommendations

Info

$(Microsoft PowerPoint - Lecci\363n 2_07.ppt)$

36 MC Lucybefore breeding represents a major physiological differencebetween cows and sows. Cattle in poor bodycondition or cows failing to increase body conditionduring lactation have low blood IGF-I during thebreeding period (Chagas et al. 2007). Sows that areunderfed during lactation have low blood IGF-I concentrationsbut blood IGF-I normalizes rapidly afterweaning if sows are fed properly. Underfeeding afterweaning in sows will suppress IGF-I, compromisefollicular development (prolonged weaning to oestrusintervals and reduced ovulation rate), and reduceembryonic survival (Zak et al. 1997). Underfeedingafter weaning, however, would be an atypical managementpractice in swine herds. In lactating dairy cows,low IGF-I would be a typical situation because lowIGF-I and high GH are favourable for milk production(Chagas et al. 2007).Under normal physiological conditions, a thresholdof IGF-I protein in follicular fluid may be met by localovarian (paracrine ⁄ autocrine) and endocrine sources ofIGF-I. According to the somatomedin hypothesis,nutritionally induced changes in liver IGF-I secretionhave a direct effect on the ovary through the endocrineactions of IGF-I. Sows and cows that are nutritionallycompromised have low concentrations of insulin andIGF-I in their blood. The lower insulin and IGF-Iconcentrations theoretically reduce ovarian responsivenessto gonadotropins (see below). At the same time,post-partum cows and weaned sows have low blood LHconcentrations, in part because of the effects of metabolichormones on GnRH secretion from the hypothalamus.Thus, the effects of nutrition on reproduction aremanifested at the ovary and at the hypothalamus andpituitary. Overcoming one limitation will not necessarilyrecover ovarian function. Responses to metabolic hormonesand gonadotropins typically follow a plateaumodel where further improvement in reproductivefunction is not seen once a critical threshold of hormoneconcentration is achieved.Local expression of IGFs and their binding proteinsInsulin-like growth factors and their binding proteinsare expressed within specific cell layers [granulosa and(or) theca] of developing follicles. This pararine ⁄ autocrinesynthesis of the IGF has been well-studied andwill not be extensively reviewed here. The reader isreferred to previous reviews on this topic for pigs andcattle (Liu et al. 2000b; Lucy 2000, 2007; Prunier andQuesnel 2000; Lucy et al. 2001b; Webb et al. 2004).There are two types of IGF, IGF-I and IGF-II, butIGF-I is the primary IGF under metabolic control. Theporcine follicle expresses IGF-I (granulosa cell layer)and IGF-II (theca cell layer). Likewise for the cow,theca cells express IGF-II. Expression of IGF-I inbovine granulosa cells has been reported by some butnot all laboratories (Webb et al. 2004). The IGF-I and-II bind to specific receptors (type I and type II IGFreceptors). The type I IGF receptor is closely related tothe insulin receptor. Both insulin and type I IGFreceptors are receptor tyrosine kinases and bothreceptors signal through related intracellular pathways.The type II IGF receptor is an unusual receptorbecause its primary function is to bind, internalize anddegrade IGF-II. In the pig, granulosa and theca cellsexpress insulin receptors as well as type I and type IIIGF receptors. Thus, insulin and IGF-I can act directlyon ovarian cells in pigs. For the cow, there is type IIGF receptor expression in the granulosa cells and typeII IGF receptor expression in granulosa and thecacells. The IGFs (but not insulin) are bound to at leastsix different binding proteins (IGFBP). Each bindingprotein has its own unique physiology. Within thebovine and porcine ovary, IGFBP-2 and -4 areexpressed and are regulators of IGF function (Fortuneet al. 2004).Ovarian follicles contain GHR mRNA and protein(Lucy 2000). In liver, GH acts on the GHR and causesan increase in hepatic IGF-I synthesis and secretion. If asimilar mechanism exists in the ovary of cows and sowsthen GH, acting directly on ovarian follicles, couldaffect ovarian function by simulating the local productionof IGF-I. Growth hormone-dependent, ovarianIGF-I synthesis has been shown in the pig (Hsu andHammond 1987). In cattle, however, GH failed toincrease ovarian IGF-I synthesis (Kirby et al. 1996).The bovine study, however, measured IGF-I mRNA inwhole ovaries. Subtle changes in IGF-I gene expressionthat may have occurred in ovarian follicles may not havebeen detected.Synergism between insulin-like growth factors andgonadotropinsAt the ovarian level, follicular growth in both cows andsows depends on LH and FSH and also insulin andIGF-I. The independent contribution of each hormoneis difficult to establish, however, because there arecoordinated changes in each of these hormones whennutrition is improved. Insulin and IGF-I can act at thelevel of the hypothalamus to stimulate GnRH secretionand therefore control the release of LH and FSH (Lucy2003; Daftary and Gore 2005). Hypothetically, mechanismsthat increase LH pulsatility through their actionson the hypothalamus and pituitary also affect theresponsiveness of the ovary to gonadotropins. Forexample, LH pulsatility increases in cows during thepost-partum period. Both insulin and IGF-I concentrationsin blood increase as well. The collective effects ofLH, insulin and IGF-I acting on the ovary promotefollicular development and ovulation.The location of specific components of the IGFsystem corresponds to the location of LH and FSHreceptors within the developing follicles. The co-localizationof IGF and gonadotropin receptor genes suggestsa coordination of gonadotropin and IGF actionwithin ovary. There is a synergistic relationship betweenthe IGFs and insulin with gonadotropins for a variety ofcellular functions including mitogenesis and steroidogenesis(Lucy 2000, 2007; Webb et al. 2004). Thesynergism is caused by the ability of IGFs and insulinto increase gonadotropin receptor numbers and increasethe activity of gonadotropin receptor second messengersystems. At the same time, gonadotropins increase type IIGF receptor expression and may increase IGF-Isynthesis in granulosa cells.Ó 2008 The Author. Journal compilation Ó 2008 Blackwell Verlag
GH and IGF-I in Cattle and Pigs 37Both insulin and IGF-I may play a role in folliculardevelopment during periods of under-feeding or weightloss because undernutrition causes a decrease in bloodconcentrations of IGF-I and insulin. According to awidely held hypothesis, blood insulin and IGF-I act inan endocrine manner to affect ovarian cells. Thedecrease in blood IGF-I and insulin concentrationsduring undernutrition decreases the responsiveness ofthe ovary to gonadotropins which ultimately leads to adecrease in follicular growth. Cosgrove et al. (1992)found that re-alimentation of feed-restricted gilts couldincrease follicular growth in the absence of a change inLH secretion. The change in follicular development wasassociated with greater plasma IGF-I and insulin in there-alimented group. Thus, feeding increases the responsivenessof the ovary to LH through its effects on insulinand IGF-I.Carry-over effects of lactation in sowsBeef and dairy cows are inseminated while they arelactating so there may not be appreciable changes inblood insulin and IGF-I before the breeding period.Sows are weaned approximately 1 week before breedingand weaning has a large effect on the metabolism of thesow and blood concentrations of insulin and IGF-I(discussed in previous section). The blood IGF-I concentrationsare normalized within approximately 3 daysafter weaning. Nonetheless, there appear to be carryovereffects of lactation. Thus, a compromised state ofovarian follicular development that develops duringlactation can potentially influence follicular growth andthe time of oestrus after weaning. Evidence for thisevolved from a variety of studies including those offollicular development before and after weaning in sows(Lucy et al. 2001b). Sows with the shortest intervals toovulation had larger follicles shortly after weaning. Inthese same sows (those with the shortest interval toovulation), there was also greater estrogenic activity offollicles before weaning and an earlier rise in preovulatoryoestradiol after weaning. Based on these data, itappears that some component of the follicular developmentafter weaning is controlled by physiologicalprocesses during lactation that affect the ovarian follicularpopulations. These physiological processes probablyinvolve gonadotropins as well as key metabolichormones like GH, insulin and IGF-I that affectgonadotropin action at the level of the ovary.Summary and ConclusionsGrowth hormone, IGF-I and insulin are metabolichormones that control growth and lactation in cattleand swine. Cows and sows typically enter into negativeenergy balance during lactation and this negative energybalance is associated with low concentrations of insulinand IGF-I in the blood. Insulin and IGF-I affect thereproductive axis through direct effects on ovarian cellsand also through their effects on gonadotropin secretionand gonadotropin receptor function. Understanding themechanisms through which metabolic hormones controlovarian function may lead to improved reproductivemanagement of both cattle and pigs because lactationand post-partum reproduction are closely tied in bothspecies.AcknowledgementsThe author would like to thank Dr Tim Safranski and AmandaWilliams of the University of Missouri for their helpful suggestionsduring the preparation of this manuscript.ReferencesAherne FX, Williams IH, 1992: Nutrition for optimizingbreeding herd performance. Vet Clin N Am Food AnimPract 8, 589–608.Bauman DE, 1999: Bovine somatotropin and lactation: frombasic science to commercial application. Domest AnimEndocrinol 17, 101–116.Bell AW, 1995: Regulation of organic nutrient metabolismduring transition from late pregnancy to early lactation. JAnim Sci 73, 2804–2819.de Braganca MM, Prunier A, 1999: Effects of low feed intakeand hot environment on plasma profiles of glucose, nonesterifiedfatty acids, insulin, glucagon, and IGF-I in lactatingsows. Domest Anim Endocrinol 16, 89–101.Brameld JM, Atkinson JL, Saunders JC, Pell JM, Buttery PJ,Gilmour RS, 1996: Effects of growth hormone administrationand dietary protein intake on insulin-like growth factorI and growth hormone receptor mRNA expression inporcine liver, skeletal muscle, and adipose tissue. J AnimSci 74, 1832–1841.van den Brand H, Prunier A, Soede NM, Kemp B, 2001: Inprimiparous sows, plasma insulin-like growth factor-I canbe affected by lactational feed intake and dietary energysource and is associated with luteinizing hormone. ReprodNutr Dev 41, 27–39.Butler ST, Marr AL, Pelton SH, Radcliff RP, Lucy MC, ButlerWR, 2003: Insulin restores GH responsiveness duringlactation-induced negative energy balance in dairy cattle:effects on expression of IGF-I and GH receptor 1A.J Endocrinol 176, 205–217.Chagas LM, Bass JJ, Blache D, Burke CR, Kay JK, LindsayDR, Lucy MC, Martin GB, Meier S, Rhodes FM, RocheJR, Thatcher WW, Webb R, 2007: Invited review: newperspectives on the roles of nutrition and metabolic prioritiesin the subfertility of high-producing dairy cows. J DairySci 90, 4022–4032.Combes S, Louveau I, Bonneau M, 1997: Moderate foodrestriction affects skeletal muscle and liver growth hormonereceptors differently in pigs. J Nutr 127, 1944–1949.Cosgrove JR, Tilton JE, Hunter MG, Foxcroft GR, 1992:Gonadotropin-independent mechanisms participate in ovarianresponses to realimentation in feed-restricted prepubertalgilts. Biol Reprod 47, 736–745.Daftary SS, Gore AC, 2005: IGF-1 in the brain as a regulatorof reproductive neuroendocrine function. Exp Biol Med(Maywood) 230, 292–306.Dauncey MJ, Burton KA, White P, Harrison AP, Gilmour RS,Duchamp C, Cattaneo D, 1994: Nutritional regulation ofgrowth hormone receptor gene expression. FASEB J 8, 81–88.Drackley JK, 1999: ADSA Foundation Scholar Award.Biology of dairy cows during the transition period: the finalfrontier?. J Dairy Sci 82, 2259–2273.Drackley JK, Donkin SS, Reynolds CK, 2006: Major advancesin fundamental dairy cattle nutrition. J Dairy Sci 89, 1324–1336.Etherton TD, Bauman DE, 1998: Biology of somatotropin ingrowth and lactation of domestic animals. Physiol Rev 78,745–761.Ó 2008 The Author. Journal compilation Ó 2008 Blackwell Verlag
Page 2 and 3: Reproduction in Domestic AnimalsOff
Page 5 and 6: Reproductionin Domestic AnimalsTabl
Page 7 and 8: Minitüb:ProductsforArtificial Inse
Page 9 and 10: Reprod Dom Anim 43 (Suppl. 2), 1-7
Page 11 and 12: Embryo Biotechnologies in Farm Anim
Page 17 and 18: Ethical Models for Studying Reprodu
Page 25 and 26: Dietary Pollutants as Risk Factors
Page 31 and 32: Reprod Dom Anim 43 (Supp. 2), 23-30
Page 33 and 34: Factors Influencing Reproduction in
Page 41 and 42: GH and IGF-I in Cattle and Pigs 33h
Page 43: GH and IGF-I in Cattle and Pigs 35h
Page 47: GH and IGF-I in Cattle and Pigs 39R
Page 51 and 52: Seasonality of Reproduction in Mamm
Page 57 and 58: Dominant Follicle Selection in Cows
Page 67 and 68: Regulation of Luteal Function 59and
Page 69 and 70: Regulation of Luteal Function 61bov
Page 71 and 72: Regulation of Luteal Function 63(+/
Page 73 and 74: Regulation of Luteal Function 65sys
Page 75 and 76: Captive Breeding of Cheetahs in Sou
Page 83 and 84: Non-invasive Monitoring of Hormones
Page 93 and 94: Biotechnology Methods for Preservin
Page 95 and 96:
Biotechnology Methods for Preservin
Page 97 and 98:
Reprod Dom Anim 43 (Suppl. 2), 89-9
Page 99 and 100:
Genetic Improvement of Dairy Cow Re
Page 101 and 102:
Page 103 and 104:
Page 105 and 106:
Nutrient Prioritization and Fertili
Page 107 and 108:
Page 109 and 110:
Page 111 and 112:
Page 113 and 114:
CL-Endometrium-Embryo Interactions
Page 115 and 116:
Page 117 and 118:
Page 119 and 120:
Page 121 and 122:
Reprod Dom Anim 43 (Suppl. 2), 113-
Page 123 and 124:
Reproductive Status Assessed by Mil
Page 125 and 126:
Page 127 and 128:
Page 129 and 130:
Page 131 and 132:
Genetic Aspects of Reproduction in
Page 133 and 134:
Page 135 and 136:
Page 137 and 138:
Page 139 and 140:
Nutritional Interactions and Reprod
Page 141 and 142:
Page 143 and 144:
Page 145 and 146:
Page 147 and 148:
Developmental Capabilities of Prepu
Page 149 and 150:
Page 151 and 152:
Page 153 and 154:
Reproductive Physiology, Pathology
Page 155 and 156:
Page 157 and 158:
Page 159 and 160:
Reproduction of Domestic Ferret 151
Page 161 and 162:
Page 163 and 164:
Page 165 and 166:
Page 167 and 168:
Canine Anoestrus, Oestrous Inductio
Page 169 and 170:
Page 171 and 172:
Page 173 and 174:
Page 175 and 176:
The Ethics and Role of AI in Dogs 1
Page 177 and 178:
Page 179 and 180:
Page 181 and 182:
Control of Fertility in Females by
Page 183 and 184:
Page 185 and 186:
Page 187 and 188:
Page 189 and 190:
Controlling Animal Populations Usin
Page 191 and 192:
Page 193 and 194:
Page 195 and 196:
Recombinant Gonadotropins in Assist
Page 197 and 198:
Page 199 and 200:
Page 201 and 202:
Page 203 and 204:
Farm Animals Embryonic Stem Cells 1
Page 205 and 206:
Page 207 and 208:
Page 209 and 210:
Reproduction in Domestic Buffalo 20
Page 211 and 212:
Page 213 and 214:
Page 215 and 216:
Page 217 and 218:
Postpartum Ovarian Activity in Sout
Page 219 and 220:
Postpartum Ovarian Activity in Sout
Page 221 and 222:
Page 223 and 224:
Mother-Offspring Interactions 215an
Page 225 and 226:
Page 227 and 228:
Reproduction Augmentation in Yak an
Page 229 and 230:
Page 231 and 232:
Page 233 and 234:
Follicles and Mares 2251982). Simil
Page 235 and 236:
Follicles and Mares 227Studies invo
Page 237 and 238:
Follicles and Mares 229dominant fol
Page 239 and 240:
Follicles and Mares 231trus, spring
Page 241 and 242:
Proteins in Early Equine Conceptuse
Page 243 and 244:
Page 245 and 246:
Page 247 and 248:
Follicular and Oocyte Competence un
Page 249 and 250:
Page 251 and 252:
Page 253 and 254:
Page 255 and 256:
Fertilization in the Porcine Fallop
Page 257 and 258:
Page 259 and 260:
Page 261 and 262:
Mastitis in Post-Partum Dairy Cows
Page 263 and 264:
Page 265 and 266:
Page 267 and 268:
Page 269 and 270:
Embryo ⁄ Foetal Losses in Ruminan
Page 271 and 272:
Page 273 and 274:
Page 275 and 276:
Page 277 and 278:
Death Ligand and Receptor Pig Ovari
Page 279 and 280:
Death Ligand and Receptor Pig Ovari
Page 281 and 282:
Page 283:
Lactocrine Programming of Uterine D
Page 286 and 287:
278 FF Bartol, AA Wiley and CA Bagn
Page 288 and 289:
Page 290 and 291:
282 KC Caires, JA Schmidt, AP Olive
Page 292 and 293:
Page 294 and 295:
Page 296 and 297:
Page 298 and 299:
290 I Dobrinskisuccessful also betw
Page 300 and 301:
292 I DobrinskiCreemers LB, Meng X,
Page 302 and 303:
294 I DobrinskiOkutsu T, Suzuki K,
Page 304 and 305:
296 N Rawlings, ACO Evans, RK Chand
Page 306 and 307:
Page 308 and 309:
Page 310 and 311:
Page 312 and 313:
304 A Dinnyes, XC Tian and X Yanggr
Page 314 and 315:
306 A Dinnyes, XC Tian and X YangIn
Page 316 and 317:
308 A Dinnyes, XC Tian and X YangHo
Page 318 and 319:
Page 320 and 321:
312 RC Bott, DT Clopton and AS Cupp
Page 322 and 323:
Page 324 and 325:
Page 326 and 327:
318 BK Whitlock, JA Daniel, RR Wilb
Page 328 and 329:
Page 330 and 331:
Page 332 and 333:
Page 334 and 335:
326 CR Barb, GJ Hausman and CA Lent
Page 336 and 337:
Page 338 and 339:
Page 340 and 341:
332 C Galli, I Lagutina, R Duchi, S
Page 342 and 343:
Page 344 and 345:
Page 346 and 347:
Page 348 and 349:
340 D Rath and LA JohnsonCommercial
Page 350 and 351:
342 D Rath and LA JohnsonThe Commer
Page 352 and 353:
344 D Rath and LA JohnsonX- and Y-b
Page 354 and 355:
346 D Rath and LA JohnsonWalker SK,
Page 356 and 357:
348 JM Vazquez, J Roca, MA Gil, C C
Page 358 and 359:
Page 360 and 361:
Page 362 and 363:
Page 364 and 365:
356 CBA Whitelaw, SG Lillico and T
Page 366 and 367:
358 CBA Whitelaw, SG Lillico and T
Page 368 and 369:
360 ACO Evans, N Forde, GM O’Gorm
Page 370 and 371:
Page 372 and 373:
Page 374 and 375:
Page 376 and 377:
Page 378 and 379:
370 JP Kastelic and JC Thundathilsp
Page 380 and 381:
372 JP Kastelic and JC Thundathilme
Page 382 and 383:
Page 384 and 385:
376 GC AlthouseTable 1. Potential s
Page 386 and 387:
378 GC Althousesemen to the domesti
Page 388 and 389:
380 B Leboeuf, JA Delgadillo, E Man
Page 390 and 391:
Page 392 and 393:
Page 394 and 395:
Page 396 and 397:
388 N Kostereva and M-C HofmannFig.
Page 398 and 399:
390 N Kostereva and M-C HofmannMMPs
Page 400 and 401:
392 N Kostereva and M-C HofmannTado
Page 402 and 403:
394 P Mermillod, R Dalbie` s-Tran,
Page 404 and 405:
Page 406 and 407:
Page 408 and 409:
Page 410 and 411:
402 K Kikuchi, N Kashiwazaki, T Nag
Page 412 and 413:
Page 414 and 415:
Page 416 and 417:
408 B ObackNumber of publications20
Page 418 and 419:
410 B ObackReprogramming Ability of
Page 420 and 421:
412 B Obackstudies have shown that
Page 422 and 423:
414 B ObackFig. 4. Climbing mount e
Page 424 and 425:
416 B ObackRenard JP, Maruotti J, J
Page 426 and 427:
418 P Loi, K Matzukawa, G Ptak, Y N
Page 428 and 429:
Page 430 and 431:
Page 434:
Table of Contents Volume 43 · Supp
show all

Reproduction in Domestic Animals

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?