ARTIFICIAL INSEMINATION IN FARM ANIMALS - Phenix-Vet

More documents

Recommendations

Info

272Artificial Insemination in Farm AnimalsThe remaining follicles are less likely to function normally, which may lead to erraticfollicular development and dysregulation of folliculogenesis (Whiteman MK, et al., 2003,Schwingl PJ, et al., 1994). Although FSH and estradiol vary near menopause, steroidogenicenzymes appear to be completely absent in the postmenopausal ovary after all functionalfollicles are lost (Couzinet B, et al., 2001). Between the ages of 20 and 40 years,concentrations of total testosterone have been reported to fall by about 50% (Zumoff B, et al.,1995). This age-related decline does not change further during the transition years (BurgerHG, et al., 2000). Similarly, dehydroepiandosterone (DHEA) and its sulphate, DHEAS,decline with age (Rossmanith W et al., 1991., Santoro N, et al., 1998). Because circulating sexhormone–binding globulin (SHBG) decreases across the menopausal transition, freeandrogen levels actually rise, as indicated by a small increase in free androgen index (T ÷SHBG × 100) (Burger HG, et al., 2000). Androstenedione, which remains relatively stableduring the transition, is converted to estrone in extra-glandular tissue. This accounts foralmost all the estrogen in circulation after menopause.When ovulation stops, concurrent with a woman's FMP, serum progesterone levels areinvariably low (Rannevik G, et al., 1995). Luteinizing hormone (LH) eventually increases,although at a slower rate than FSH. Despite the epidemiologic trend toward elevated FSHand decreased estradiol with progression through the transition, measurement of FSH,inhibin, and estradiol provides at best an unreliable guide to the menopausal status of anindividual woman (El-Hage G, et al., 2007; Braunstein GD, et al., 2005). A more rationalapproach to diagnosing menopause would include an assessment of the longitudinalsymptoms of a woman who presents with peri-menopausal complaints (Lobo RA., 1999).Hormone profiles correlate well with symptoms and cycle features (Burger HD, et al., 1995).Thus, if a woman is >45 years old and has had a recent disruption in her menstrual patternand symptoms suggestive of transient hypo-estrogenemia, it is likely that she has enteredher menopausal transition (Santoro N., 2002). That being said, the clinician should take careto rule out other pathologies that can be masked by common complaints associated with themenopausal transition. At minimum, a screening TSH level should be performed, asmenstrual irregularity may be the only manifestation of thyroid dysfunction.4. Regulation of gonadotropins and control of ovarian steroid productionPituitary gonadotropes synthesize and secrete both LH and FSH. They account for 7% to15% of anterior pituitary cells. Gonadotropin subunit gene expression is regulated by thefrequency of GnRH signal input to pituitary gonadotropes (Haisenleder DJ, et al., 1991).During the menstrual cycle, LH pulse frequency is approximately every 90 minutes in theearly follicular phase, 60 to 70 minutes during the late follicular phase, 100 minutes duringthe early luteal phase, and 200 minutes during the late luteal phase. This variation reflectschanges in GnRH pulse frequency, which regulates relative FSH and LH secretion; this, inturn, determines follicle recruitment, development, and ovulation. More rapid GnRH pulsefrequencies promote LH secretion, and slower frequencies promote FSH secretion. Althoughgood evidence indicates that changes in GnRH pulse frequency determines differential LHand FSH secretion (Marshall JC, et al., 1993) it is apparent that ovarian steroids and peptidehormones have a major role. Women with hypothalamic stalk section regain theircharacteristic cycle length when administered an unchanging frequency of exogenousGnRH pulses every 90 minutes.
Reproductive Endocrinology Diseases: Hormone Replacement and Therapy for Peri/Menopause 273This indicates that intrinsic rates of follicle development and regression of the corpusluteum, along with their phasing of steroid and peptide hormone production, are majordeterminants of LH and FSH responses to GnRH. Gonadotropins control the growth anddifferentiation of the steroid hormone–secreting cells of the ovary, intrinsically linking formand function. A defined sequence of gonadotropin action propels the growth of follicles andthe production of steroid hormones. Positive feedback on the pituitary by highconcentrations of estrogens leads to the ovulatory surge of LH, which in turn triggers adramatic differentiation event, resulting in structural reorganization of the pre-ovulatoryfollicle, release of the ovum, and striking changes in the steroidogenic capacity of theluteinizing cells. Follicular growth, which culminates in ovulation and corpus luteumformation, requires both FSH and LH. Steroidogenic competence of the ovarian follicle is notachieved in the absence of FSH, even if LH is present in abundance. FSH promotesproliferation of the granulosa cells and induces the expression of genes involved in estradiolbiosynthesis (Haisenleder DJ, et al., 1991; Kaiser UB, et al., 1997). During the last phase offollicular maturation, when granulosa cells acquire LH receptors, LH is then able to sustainfollicular estradiol synthesis. This LH substitution is thought to compensate for thediminished levels of FSH of the late follicular phase consequent to negative-feedback actionof estradiol and inhibin. LH action on the granulosa thus rescues the dominant LHexpressingfollicle from the fate of atresia. LH stimulation is indispensable for normalovarian hormone production not only before but also after ovulation. Suppression of LHrelease leads to a prompt decline in progesterone levels that precede changes in theabundance of mRNAs encoding steroidogenic enzymes or structural changes in the corpusluteum (King JA & Millar RP., 1982).This acute regulation of ovarian progesterone secretion is controlled by LH via theexpression of steroidogenic acute regulatory protein (StAR) messenger RNA (mRNA) andprotein, present in both theca-lutein and granulosa-lutein cells throughout the luteal phaseare highly expressed in early and midluteal phase, whereas declining StAR mRNA andprotein levels are characteristic of late luteal phase. Moreover, StAR protein levels in thecorpus luteum are highly correlated with plasma progesterone levels; suppression of LHlevels during the midluteal phase markedly decreases plasma progesterone levels andabundance of StAR mRNA transcripts in the corpus luteum (Millar RP, et al., 2004).4.1 Intra-ovarian control mechanismsThe growth of follicles and the function of the corpus luteum, while under the primarydirection of the pituitary, are highly influenced by intra-ovarian factors that modulate theaction of gonadotropins. These intra-ovarian factors most likely account for gonadotropinindependentfollicular growth, observed differences in the rate and extent of developmentof ovarian follicles, arrest and initiation of meiosis, dominant follicle selection, andluteolysis. The list of potential paracrine factors that can influence steroid production bytheca and granulosa cells is long and diverse. The previous theca cells lacked the aromataseenzyme that is necessary to produce estrogen (Schwanzel-Fukuda M, & Pfaff DW, 1984) sothe production of estrogen in granulosa cells indicates presence of aromatase. It includesvarious growth factors, cytokines, peptide hormones, and steroids such as epidermalgrowth factor, transforming growth factor β (TGF-β), platelet-derived growth factor,fibroblast growth factors, transforming growth factor α (TGF-α), activins, inhibins, Anti-Müllerian hormone, insulin-like growth factors, estradiol, progesterone, and GnRH (MillarR: 2005; King JA, et al., 2002)
Page 3 and 4:
VIContentsChapter 9Evaluation of a
Page 5:
XPrefaceless stress to the female,
Page 8 and 9:
2Artificial Insemination in Farm An
Page 10 and 11:
Page 12 and 13:
Page 14 and 15:
Page 16 and 17:
10Artificial Insemination in Farm A
Page 18 and 19:
Page 20 and 21:
Page 22 and 23:
Page 24 and 25:
Page 26 and 27:
Page 28 and 29:
Page 30 and 31:
Page 32 and 33:
Page 34 and 35:
Page 36 and 37:
Page 38 and 39:
Page 40 and 41:
Page 42 and 43:
Page 44 and 45:
Page 46 and 47:
Page 48 and 49:
Page 50 and 51:
Page 52 and 53:
Page 54 and 55:
Page 56 and 57:
Page 58 and 59:
Page 60 and 61:
Page 62 and 63:
Page 64 and 65:
Page 66 and 67:
Page 68 and 69:
Page 70 and 71:
Page 72 and 73:
Page 74 and 75:
Page 76 and 77:
Page 78 and 79:
Page 80 and 81:
Page 82 and 83:
Page 84 and 85:
Page 86 and 87:
Page 88 and 89:
Page 90 and 91:
Page 92 and 93:
Page 94 and 95:
Page 96 and 97:
Page 98 and 99:
Page 100 and 101:
Page 102 and 103:
Page 104 and 105:
Page 106 and 107:
100Artificial Insemination in Farm
Page 108 and 109:
Page 110 and 111:
Page 112 and 113:
Page 114 and 115:
Page 116 and 117:
Page 118 and 119:
Page 120 and 121:
Page 122 and 123:
Page 124 and 125:
Page 126 and 127:
Page 128 and 129:
Page 130 and 131:
Page 132 and 133:
Page 134 and 135:
Page 136 and 137:
Page 138 and 139:
Page 140 and 141:
Page 142 and 143:
Page 144 and 145:
Page 146 and 147:
Page 148 and 149:
Page 150 and 151:
Page 152 and 153:
Page 154 and 155:
Page 156 and 157:
Page 158 and 159:
Page 160 and 161:
Page 162 and 163:
Page 164 and 165:
Page 166 and 167:
Page 168 and 169:
Page 170 and 171:
Page 172 and 173:
Page 174 and 175:
Page 176 and 177:
Page 178 and 179:
Page 180 and 181:
Page 182 and 183:
Page 184 and 185:
Page 186 and 187:
Page 188 and 189:
Page 190 and 191:
Page 192 and 193:
Page 194 and 195:
Page 196 and 197:
Page 198 and 199:
Page 200 and 201:
Page 202 and 203:
Page 204 and 205:
Page 206 and 207:
Page 208 and 209:
Page 210 and 211:
Page 212 and 213:
Page 214 and 215:
Page 216 and 217:
Page 218 and 219:
Page 220 and 221:
Page 222 and 223:
Page 224 and 225:
Page 226 and 227:
Page 228 and 229: 222Artificial Insemination in Farm
Page 306: 300Artificial Insemination in Farm
show all

ARTIFICIAL INSEMINATION IN FARM ANIMALS - Phenix-Vet

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

Delete template?

Save as template?