There is sparse research literature in agricultural economics regarding early weaning as a potential alternative production/marketing strategy. The objective of this research is to estimate and analyze the impacts on net returns of alternative weaning dates for Tennessee cow-calf operations including alternative post-weaning treatments for calves. The Decision Evaluator for the Cattle Industry (DECI) simulation program was used for this study to produce outputs such as calf numbers, gender, and weights, other output including cow weights and body condition score, both at calving and at weaning, and pregnancy percentages. Forty-two simulations were run for average and summer drought weather, weaning at an average age of 135, 165, 195, 225, 255, and 285 days and selling at weaning or after a 60 or 90-day drylot backgrounding period. Prices for steers, heifers, and culled cows from 1995-2008 were taken from market reports. Costs were derived from University of Tennessee Extension Beef and Forage Budgets and USDA-NASS. The outputs from DECI were combined with prices to result in total revenues. Subtracting the costs of feed, interest, veterinary and medical, and marketing resulted in return to land, labor, management, and risk to the enterprise. The results of this study revealed that under average weather conditions in East Tennessee, marketing at weaning in November yielded the highest net return. Weaning in August and backgrounding for 60 days yielded the lowest net return with the base 90-cow herd. Under summer drought conditions, marketing at weaning in August resulted in the highest net return. Weaning in November and marketing after a 90-day backgrounding period yielded the lowest net return. Under the conditions used in this study, the only time early weaning makes economic sense is when herd size is increased for June or July weaning or under drought conditions when August (195 days) weaning and sale is optimal. Several limitations of this study imply that additional research is required on this topic before definite conclusions can be drawn.

There is sparse research literature in agricultural economics regarding early weaning as a potential alternative production/marketing strategy. The objective of this research is to estimate and analyze the impacts on net returns of alternative weaning dates for Tennessee cow-calf operations including alternative post-weaning treatments for calves.The Decision Evaluator for the Cattle Industry (DECI) simulation program was used for this study to produce outputs such as calf numbers, gender, and weights, other output including cow weights and body condition score, both at calving and at weaning, and pregnancy percentages. Forty-two simulations were run for average and summer drought weather, weaning at an average age of 135, 165, 195, 225, 255, and 285 days and selling at weaning or after a 60 or 90-day drylot backgrounding period. Prices for steers, heifers, and culled cows from 1995-2008 were taken from market reports. Costs were derived from University of Tennessee Extension Beef and Forage Budgets and USDA-NASS. The outputs from DECI were combined with prices to result in total revenues. Subtracting the costs of feed, interest, veterinary and medical, and marketing resulted in return to land, labor, management, and risk to the enterprise. The results of this study revealed that under average weather conditions in East Tennessee, marketing at weaning in November yielded the highest net return. Weaning in August and backgrounding for 60 days yielded the lowest net return with the base 90-cow herd.Under summer drought conditions, marketing at weaning in August resulted in the highest net return. Weaning in November and marketing after a 90-day backgrounding period yielded the lowest net return.Under the conditions used in this study, the only time early weaning makes economic sense is when herd size is increased for June or July weaning or under drought conditions when August (195 days) weaning and sale is optimal. Several limitations of this study imply that additional research is required on this topic before definite conclusions can be drawn.

Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro / O desmame precoce (DP) leva ao desenvolvimento tardio de obesidade e de resistência insulínica (RI), sendo essas alterações prevenidas quando os animais são suplementados com cálcio. Sabe-se que os peptídeos gastrointestinais (GI) atuam na regulação do apetite e em diversos outros processos, podendo ter um papel relevante no desenvolvimento da obesidade e RI. Uma vez que os animais programados pelo DP são obesos e hiperfágicos, investigamos o perfil plasmático e tecidual de GLP-1, CCK e PYY (anorexígenos) de grelina (orexígena) e de seus receptores, assim como o efeito da dieta rica em cálcio sobre estes peptídeos a fim de identificar algum distúrbio no controle do apetite. Ao nascimento das proles, ratas lactantes Wistar foram separadas em: grupo DP (desmame precoce, n=20), filhotes cujas mães tiveram as mamas enfaixadas, impedindo o acesso da prole ao leite nos últimos 3 dias de lactação; e grupo C (controle, n=10), filhotes com livre acesso ao leite materno. Aos 120 dias, as proles DP foram subdivididas em: grupo DP, alimentado com ração comercial padrão, e grupo DPCa, alimentado com ração suplementada com cálcio (10g de carbonato de cálcio/Kg de ração). Os animais foram sacrificados aos 21 e 180 dias de vida. Quantificamos: GLP-1, CCK, PYY, grelina e citocinas (IL-6, TNF-&#945; e IL-10) plasmáticas por ELISA; o conteúdo de grelina no estômago por ELISA e imunohistoquímica; o conteúdo de GLP-1 (intestino), GLP1-R (intestino, TA e ARC) e GHSR-1a (estômago e ARC) por Western blotting. Dados significativos quando p<0,05. Aos 21 dias, a prole DP apresentou aumento de GLP-1 no plasma (+168%) e GLP1-R no tecido adiposo (+72%), embora menor conteúdo de GLP-1 (-59%) e GLP1-R (-58%) no intestino. Não observamos alterações plasmáticas de grelina, CCK e PPY e no conteúdo de GHSR-1a no estômago aos 21 dias. Aos 180 dias, não verificamos diferença em nenhum dos peptídeos GI no plasma na prole DP. Porém, observamos menor conteúdo intestinal de GLP-1 tanto no grupo DP (-33%) quanto no DPCa (-32%), e uma tendência da grelina (+20%) e do GHSR-1a (+31%) a estarem elevados no estômago do grupo DP. Além de menor conteúdo de GLP1-R no tecido adiposo no grupo DP (-59%) e maior conteúdo de GLP1-R no intestino da prole DPCa (+62%). Não encontramos diferença entre os grupos na expressão de GLP1-R e GHSR-1a no ARC. O grupo DP apresentou ainda um perfil pró-inflamatório caracterizado por maior TNF-&#945; e menor IL-10 no plasma. O DP alterou o perfil dos peptídeos GI a curto e longo prazos, o que pode ter colaborado para o desenvolvimento da obesidade, hiperfagia e RI neste modelo, uma vez que o GLP-1, único peptídeo alterado no período de imprinting, possui um possível papel adipogênico. A suplementação com cálcio foi capaz de reverter todas as alterações produzidas pelo DP. Evidenciamos, então, a importância do aleitamento materno na formação do comportamento alimentar e do balanço metabólico, bem como o papel da suplementação com cálcio no tratamento da obesidade e seus distúrbios associados, inclusive nas alterações do apetite. / Early weaning (EW) leads to late development of obesity and insulin resistance (IR), and these changes are prevented when EW animals are supplemented with calcium. It is known that gut peptides with regulatory action upon appetite and several other processes with possible role in the obesity development and IR. As the EW programmed animals are obese and hyperphagic, in this study we evaluated plasma and tissue profile of GLP-1, CCK and PYY (anorexigenic peptides), and ghrelin (orexigenic peptide) and their receptors as well as the effects of rich calcium diet on these parameters in order to find some disturbance in the appetite control. At birth, lactating Wistar rats were separated in: EW (Early Weaning, n=20), lactating rats were involved with a bandage to interrupt the lactation during the last 3 days of standard lactation, and C (control, n=20), dams whose pups had free access to milk during all lactation (21 days). At 120 days-old, half of DP group received dietary calcium supplementation (10g of calcium carbonate/Kg of rat chow); DP and C groups received standard diet. Offspring were killed at 21 and 180 days-old. Plasma GLP-1, CCK, PYY, ghrelin and the cytokines (IL-6, TNF-&#945; and IL-10), and ghrelin content in the stomach are analyzed by ELISA; which was also examined by immunohistochemistry; GLP1 content (gut) GLP1-R (gut, adipose tissue and hypothalamus-ARC) and e GHSR-1a (stomach and hypothalamus-ARC) are evaluated by Western blotting. Significant data were p<0.05. At 21 days-old, EW group presented higher plasma GLP1 (+168%) and GLP1-R in adipose tissue (+72%), although lower GLP-1 (-59%) and GLP1-R (-58%) content in gut. We not found changes in plasma ghrelin, CCK and PYY as well as in stomach GHSR-1a content. At 180 days-old, we found no changes in plasma gastrointestinal peptides in EW offspring. However, we observed lower gut GLP1 content in both EW group (-33%) and in EWCa (-32%), and a trend of ghrelin (+20%) and GHSR-1a (+31%) to be increased in EW group. In addition, we detected lower GLP1-R content in adipose tissue in EW group (-59%) and higher gut GLP1-R content in EWCa (+62%). We found no change among groups in GLP1-R and GHSR-1a expression in the ARC. EW group also showed a proinflammatory profile characterized by higher TNF-&#945; and lower IL-10 levels. EW had short and long-term effects on the profile of gastrointestinal peptides, which may have contributed to the development of obesity, hyperphagia and IR, since GLP-1 is the unique peptide changed during the imprinting period, which has an adipogenic role. Calcium supplementation was able to prevent all changes produced by EW. We evidence the importance of breastfeeding on feeding behavior development and metabolic balance as well as the role of calcium supplementation in obesity treatment and other disorders, including changes in appetite.

Conselho Nacional de Desenvolvimento Científico e Tecnológico / A obesidade, cuja origem é multifatorial e a prevalência é crescente em diferentes regiões no mundo, está geralmente associada à produção desregulada de adipocinas, ao aumento do estresse oxidativo e à ocorrência de distúrbios metabólicos como dislipidemia, intolerância à glicose e hipertensão. A Programação Metabólica ou Plasticidade Ontogenética tem sido proposta como um importante fator na etiologia da obesidade. Este fenômeno sugere que alterações nutricionais, hormonais e ambientais durante períodos críticos do desenvolvimento, tais como gestação e lactação, podem alterar a fisiologia e o metabolismo de um organismo provocando o desenvolvimento de distúrbios metabólicos na vida adulta. Neste trabalho foram estudados dois modelos de plasticidade ontogenética que programam ratos Wistar para obesidade na vida adulta: a supernutrição na lactação e o desmame precoce. A supernutrição na lactação provocada pela redução da ninhada causou obesidade, hiperfagia, aumento do estresse oxidativo, resistência hepática à ação da insulina e esteatose nas proles na idade adulta. A desnutrição, provocada pelo desmame precoce, também se associou na idade adulta com obesidade visceral, aumento do estresse oxidativo e esteatose, assim como dislipidemia, resistência à insulina, hipertensão arterial e resistência central à leptina. No modelo de programação pelo desmame precoce, os animais adultos foram tratados com resveratrol (30mg/kg/MC), um polifenol encontrado nas uvas e conhecido por seus efeitos antioxidante e hipoglicemiante, por 30 dias. Os animais programados pelo desmame precoce que receberam resveratrol tiveram massa corporal, gordura visceral e morfologia hepática semelhantes aos animais controles. Ainda, o resveratrol normalizou a pressão arterial, a dislipidemia, a glicemia e as concentrações de adiponectina e leptina. A normalização da leptinemia esteve associada à correção da resistência central à leptina nestes animais, uma vez que o resveratrol normalizou além da ingestão, o conteúdo hipotalâmico de JAK2, pSTAT3 e NPY. Portanto, os animais programados pela supernutrição na lactação ou pelo desmame precoce apresentaram aumento do estresse oxidativo associado à obesidade e alterações metabólicas como esteatose. O tratamento com resveratrol nos animais programados pelo desmame precoce preveniu o aumento de estresse oxidativo, obesidade visceral, resistência à insulina, dislipidemia e esteatose. Além disso, o resveratrol causou normalização da leptinemia nestes animais, assim como da ação deste hormônio no hipotálamo, controlando a hiperfagia característica deste modelo. / Obesity, a multifactorial disease with increased prevalence in different regions in the world, is generally associated with a deregulated adipocytokines production, increased oxidative stress and the occurrence of metabolic disorders such as dyslipidemia, glucose intolerance and hypertension. The Metabolic Programming or Developmental Plasticity has been proposed as important factor in the etiology of obesity. This phenomenon suggests that dietary changes, hormonal and environmental factors during critical periods of development, such as pregnancy and lactation can alter the physiology and metabolism of an organism causing the development of metabolic disorders at adulthood. In this work, we studied two models of developmental plasticity in Wistar rats, which programmed for obesity at adulthood: overnutrition during lactation and early weaning. Overnutrition during lactation through litter size reduction caused obesity, hyperphagia, increased oxidative stress, liver insulin resistance and steatosis in offspring at adulthood. Malnutrition caused by early weaning was also associated with visceral obesity, increased oxidative stress and steatosis as well as dyslipidemia, insulin resistance, hypertension and central leptin resistance in adulthood. In this programming model by early weaning, adult animals were treated with resveratrol (30mg/kg/BW for 30 days), a polyphenol found in grapes and known for its antioxidant and hypoglycemic actions. Offspring programmed by early weaning that were treated with resveratrol had body mass, visceral fat and liver morphology similar to those found in control offspring. Also, resveratrol normalized blood pressure, dyslipidemia, and serum glucose, adiponectin and leptin. The normalization of leptin levels was associated with the correction of central leptin resistance in these animals, since resveratrol normalized food intake and hypothalamic content of JAK2, pSTAT3 and NPY. Therefore, offspring programmed by overnutrition during lactation or early weaning displayed increased oxidative stress, obesity and metabolic disorders such as steatosis. Treatment with resveratrol in early weaned offspring prevented the increase of oxidative stress, visceral obesity, insulin resistance, dyslipidemia and steatosis. Indeed, resveratrol normalized serum leptin as well as its action in the hypothalamus, controlling the hyperphagia characteristic of these offspring.

Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro / O desmame precoce (DP) leva ao desenvolvimento tardio de obesidade e de resistência insulínica (RI), sendo essas alterações prevenidas quando os animais são suplementados com cálcio. Sabe-se que os peptídeos gastrointestinais (GI) atuam na regulação do apetite e em diversos outros processos, podendo ter um papel relevante no desenvolvimento da obesidade e RI. Uma vez que os animais programados pelo DP são obesos e hiperfágicos, investigamos o perfil plasmático e tecidual de GLP-1, CCK e PYY (anorexígenos) de grelina (orexígena) e de seus receptores, assim como o efeito da dieta rica em cálcio sobre estes peptídeos a fim de identificar algum distúrbio no controle do apetite. Ao nascimento das proles, ratas lactantes Wistar foram separadas em: grupo DP (desmame precoce, n=20), filhotes cujas mães tiveram as mamas enfaixadas, impedindo o acesso da prole ao leite nos últimos 3 dias de lactação; e grupo C (controle, n=10), filhotes com livre acesso ao leite materno. Aos 120 dias, as proles DP foram subdivididas em: grupo DP, alimentado com ração comercial padrão, e grupo DPCa, alimentado com ração suplementada com cálcio (10g de carbonato de cálcio/Kg de ração). Os animais foram sacrificados aos 21 e 180 dias de vida. Quantificamos: GLP-1, CCK, PYY, grelina e citocinas (IL-6, TNF-&#945; e IL-10) plasmáticas por ELISA; o conteúdo de grelina no estômago por ELISA e imunohistoquímica; o conteúdo de GLP-1 (intestino), GLP1-R (intestino, TA e ARC) e GHSR-1a (estômago e ARC) por Western blotting. Dados significativos quando p<0,05. Aos 21 dias, a prole DP apresentou aumento de GLP-1 no plasma (+168%) e GLP1-R no tecido adiposo (+72%), embora menor conteúdo de GLP-1 (-59%) e GLP1-R (-58%) no intestino. Não observamos alterações plasmáticas de grelina, CCK e PPY e no conteúdo de GHSR-1a no estômago aos 21 dias. Aos 180 dias, não verificamos diferença em nenhum dos peptídeos GI no plasma na prole DP. Porém, observamos menor conteúdo intestinal de GLP-1 tanto no grupo DP (-33%) quanto no DPCa (-32%), e uma tendência da grelina (+20%) e do GHSR-1a (+31%) a estarem elevados no estômago do grupo DP. Além de menor conteúdo de GLP1-R no tecido adiposo no grupo DP (-59%) e maior conteúdo de GLP1-R no intestino da prole DPCa (+62%). Não encontramos diferença entre os grupos na expressão de GLP1-R e GHSR-1a no ARC. O grupo DP apresentou ainda um perfil pró-inflamatório caracterizado por maior TNF-&#945; e menor IL-10 no plasma. O DP alterou o perfil dos peptídeos GI a curto e longo prazos, o que pode ter colaborado para o desenvolvimento da obesidade, hiperfagia e RI neste modelo, uma vez que o GLP-1, único peptídeo alterado no período de imprinting, possui um possível papel adipogênico. A suplementação com cálcio foi capaz de reverter todas as alterações produzidas pelo DP. Evidenciamos, então, a importância do aleitamento materno na formação do comportamento alimentar e do balanço metabólico, bem como o papel da suplementação com cálcio no tratamento da obesidade e seus distúrbios associados, inclusive nas alterações do apetite. / Early weaning (EW) leads to late development of obesity and insulin resistance (IR), and these changes are prevented when EW animals are supplemented with calcium. It is known that gut peptides with regulatory action upon appetite and several other processes with possible role in the obesity development and IR. As the EW programmed animals are obese and hyperphagic, in this study we evaluated plasma and tissue profile of GLP-1, CCK and PYY (anorexigenic peptides), and ghrelin (orexigenic peptide) and their receptors as well as the effects of rich calcium diet on these parameters in order to find some disturbance in the appetite control. At birth, lactating Wistar rats were separated in: EW (Early Weaning, n=20), lactating rats were involved with a bandage to interrupt the lactation during the last 3 days of standard lactation, and C (control, n=20), dams whose pups had free access to milk during all lactation (21 days). At 120 days-old, half of DP group received dietary calcium supplementation (10g of calcium carbonate/Kg of rat chow); DP and C groups received standard diet. Offspring were killed at 21 and 180 days-old. Plasma GLP-1, CCK, PYY, ghrelin and the cytokines (IL-6, TNF-&#945; and IL-10), and ghrelin content in the stomach are analyzed by ELISA; which was also examined by immunohistochemistry; GLP1 content (gut) GLP1-R (gut, adipose tissue and hypothalamus-ARC) and e GHSR-1a (stomach and hypothalamus-ARC) are evaluated by Western blotting. Significant data were p<0.05. At 21 days-old, EW group presented higher plasma GLP1 (+168%) and GLP1-R in adipose tissue (+72%), although lower GLP-1 (-59%) and GLP1-R (-58%) content in gut. We not found changes in plasma ghrelin, CCK and PYY as well as in stomach GHSR-1a content. At 180 days-old, we found no changes in plasma gastrointestinal peptides in EW offspring. However, we observed lower gut GLP1 content in both EW group (-33%) and in EWCa (-32%), and a trend of ghrelin (+20%) and GHSR-1a (+31%) to be increased in EW group. In addition, we detected lower GLP1-R content in adipose tissue in EW group (-59%) and higher gut GLP1-R content in EWCa (+62%). We found no change among groups in GLP1-R and GHSR-1a expression in the ARC. EW group also showed a proinflammatory profile characterized by higher TNF-&#945; and lower IL-10 levels. EW had short and long-term effects on the profile of gastrointestinal peptides, which may have contributed to the development of obesity, hyperphagia and IR, since GLP-1 is the unique peptide changed during the imprinting period, which has an adipogenic role. Calcium supplementation was able to prevent all changes produced by EW. We evidence the importance of breastfeeding on feeding behavior development and metabolic balance as well as the role of calcium supplementation in obesity treatment and other disorders, including changes in appetite.

Conselho Nacional de Desenvolvimento Científico e Tecnológico / A obesidade, cuja origem é multifatorial e a prevalência é crescente em diferentes regiões no mundo, está geralmente associada à produção desregulada de adipocinas, ao aumento do estresse oxidativo e à ocorrência de distúrbios metabólicos como dislipidemia, intolerância à glicose e hipertensão. A Programação Metabólica ou Plasticidade Ontogenética tem sido proposta como um importante fator na etiologia da obesidade. Este fenômeno sugere que alterações nutricionais, hormonais e ambientais durante períodos críticos do desenvolvimento, tais como gestação e lactação, podem alterar a fisiologia e o metabolismo de um organismo provocando o desenvolvimento de distúrbios metabólicos na vida adulta. Neste trabalho foram estudados dois modelos de plasticidade ontogenética que programam ratos Wistar para obesidade na vida adulta: a supernutrição na lactação e o desmame precoce. A supernutrição na lactação provocada pela redução da ninhada causou obesidade, hiperfagia, aumento do estresse oxidativo, resistência hepática à ação da insulina e esteatose nas proles na idade adulta. A desnutrição, provocada pelo desmame precoce, também se associou na idade adulta com obesidade visceral, aumento do estresse oxidativo e esteatose, assim como dislipidemia, resistência à insulina, hipertensão arterial e resistência central à leptina. No modelo de programação pelo desmame precoce, os animais adultos foram tratados com resveratrol (30mg/kg/MC), um polifenol encontrado nas uvas e conhecido por seus efeitos antioxidante e hipoglicemiante, por 30 dias. Os animais programados pelo desmame precoce que receberam resveratrol tiveram massa corporal, gordura visceral e morfologia hepática semelhantes aos animais controles. Ainda, o resveratrol normalizou a pressão arterial, a dislipidemia, a glicemia e as concentrações de adiponectina e leptina. A normalização da leptinemia esteve associada à correção da resistência central à leptina nestes animais, uma vez que o resveratrol normalizou além da ingestão, o conteúdo hipotalâmico de JAK2, pSTAT3 e NPY. Portanto, os animais programados pela supernutrição na lactação ou pelo desmame precoce apresentaram aumento do estresse oxidativo associado à obesidade e alterações metabólicas como esteatose. O tratamento com resveratrol nos animais programados pelo desmame precoce preveniu o aumento de estresse oxidativo, obesidade visceral, resistência à insulina, dislipidemia e esteatose. Além disso, o resveratrol causou normalização da leptinemia nestes animais, assim como da ação deste hormônio no hipotálamo, controlando a hiperfagia característica deste modelo. / Obesity, a multifactorial disease with increased prevalence in different regions in the world, is generally associated with a deregulated adipocytokines production, increased oxidative stress and the occurrence of metabolic disorders such as dyslipidemia, glucose intolerance and hypertension. The Metabolic Programming or Developmental Plasticity has been proposed as important factor in the etiology of obesity. This phenomenon suggests that dietary changes, hormonal and environmental factors during critical periods of development, such as pregnancy and lactation can alter the physiology and metabolism of an organism causing the development of metabolic disorders at adulthood. In this work, we studied two models of developmental plasticity in Wistar rats, which programmed for obesity at adulthood: overnutrition during lactation and early weaning. Overnutrition during lactation through litter size reduction caused obesity, hyperphagia, increased oxidative stress, liver insulin resistance and steatosis in offspring at adulthood. Malnutrition caused by early weaning was also associated with visceral obesity, increased oxidative stress and steatosis as well as dyslipidemia, insulin resistance, hypertension and central leptin resistance in adulthood. In this programming model by early weaning, adult animals were treated with resveratrol (30mg/kg/BW for 30 days), a polyphenol found in grapes and known for its antioxidant and hypoglycemic actions. Offspring programmed by early weaning that were treated with resveratrol had body mass, visceral fat and liver morphology similar to those found in control offspring. Also, resveratrol normalized blood pressure, dyslipidemia, and serum glucose, adiponectin and leptin. The normalization of leptin levels was associated with the correction of central leptin resistance in these animals, since resveratrol normalized food intake and hypothalamic content of JAK2, pSTAT3 and NPY. Therefore, offspring programmed by overnutrition during lactation or early weaning displayed increased oxidative stress, obesity and metabolic disorders such as steatosis. Treatment with resveratrol in early weaned offspring prevented the increase of oxidative stress, visceral obesity, insulin resistance, dyslipidemia and steatosis. Indeed, resveratrol normalized serum leptin as well as its action in the hypothalamus, controlling the hyperphagia characteristic of these offspring.

O objetivo do experimento I foi avaliar a interação entre dois ganhos médios diários [GMD - fator nutricional (ganho elevado GA = 0,700 e ganho baixo GB = 0,300 Kg/dia)] e a diferença esperada da progênie (DEP para idade ao primeiro parto - fator genético) na puberdade de novilhas Nelore. Foram utilizadas 58 novilhas desmamadas com 8 meses de idade, filhas de 4 touros [2 precoces (P) e 2 tardios (T)], formando um esquema fatorial 2 x 2, no qual o fator 1 foi o GMD e o fator 2 foi a DEP do touro, constituindo assim quatro tratamentos: Touro precoce com GMD elevado (PGA), touro precoce com GMD baixo (PGB), touro tardio com GMD elevado (TGA), touro tardio com GMD baixo (TGB). Houve efeito dos tratamentos na porcentagem de novilhas púberes durante o experimento (PGA e PGB = 100%; TGA = 83% até 27 meses de idade; TGB = 38% até 3 anos de idade). As novilhas do PGA apresentaram a menor (P = 0,0001) idade na puberdade (18 &#177; 1 meses). Contudo, a nutrição atrasou a puberdade em cerca de 10 meses nas novilhas filhas de touros precoces e tardios (PGA = 18 &#177; 1 vs. PGB = 29 &#177; 1 meses; TGA = 24 &#177; 1 vs. TGB = 34 &#177; 1 meses). Assim podemos concluir que a DEP para IPP foi o fator necessário para o adiantamento da idade a puberdade. No entanto, o GMD foi um fator limitante para o aparecimento da puberdade. O objetivo do experimento II foi avaliar o efeito do imprinting metabólico dos 3 aos 7 meses de idade na puberdade em novilhas cruzadas (Angus x Nelore). Os tratamentos foram arranjados em esquema fatorial 2 x 2, no qual o fator 1 foi GMD elevado e médio dos 3 aos 7 meses de idade (fase 1) e o fator 2 foi GMD elevado e médio dos 7 meses de idade até a puberdade (fase 2). Formando os seguintes tratamentos: CAA Novilhas cruzadas submetidas ao GMD elevado nas fases 1 e 2; CAM - GMD elevado na fase 1 e GMD médio na fase 2; CMA- GMD médio na fase1 e GMD elevado na fase 2; CMM GMD médio nas fases 1 e 2. O GMD médio foi atingido pela restrição do consumo de matéria seca (CMS) no GMD médio. As novilhas dos tratamentos CAA, CAM e CMA apresentaram puberdade na mesma idade (cerca de 12 meses). As novilhas cruzadas submetidas ao GMD elevado na fase 2 foram mais pesadas (P = 0,0379) na puberdade do que novilhas submetidas ao baixo GMD. O GMD elevado dos 3 aos 7 meses de idade não impactou na puberdade das novilhas cruzadas. O objetivo e a metodologia do experimento III foram semelhantes ao experimento II, no entanto foram utilizadas novilhas Nelore (N) ao invés de cruzadas e o experimento terminou aos 19 meses de idade. O tratamento NAA (84%) induziu maior (P = 0,0145) proporção de novilhas púberes do que o NMM (23%), mas não houve diferença na taxa de puberdade entre os tratamentos NAM (60%) e NMA (50%). Além disso, o comportamento das curvas de puberdade dos tratamentos NAM e NMA foram semelhantes, sendo assim não houve efeito de imprinting metabólico nas novilhas Nelore. O GMD elevado dos 3 aos 19 meses idade aumentou a porcentagem de novilhas Nelore púberes aos 19 meses de idade / The objective of experiment I was to evaluate the interaction between two average daily gain (ADG nutritional factor (high gain HG = 0,700 and low gain LG = 0,300 kg/day)] and expected progeny differences (EPD to age at first calving; genetic factor) on puberty attainment of Nellore heifers. Fifth eight heifers weaned at 8 months of age and daughters of 4 sires [2 precocious (P) and 2 later (L)]. A factorial design 2 x 2 was used, where the factor 1 was the ADG and the factor 2 was the EPD of sire, resulting in four treatments: Precocious sire with HG (PHG), precocious sire with LG (PLG), later sire with HG (LHG) and later sire with LG (LLG). There was effect of treatment in the percentage of pubertal heifers (PHG and PLG = 100%; LHG = 83% until 27 month of age; LLG = 38% until 3 years old). Heifers from the PHG treatment were the youngest (P = 0,0001) (18 months of age). However, the nutritional factor delayed puberty achievement by approximately 10 months the age at puberty in precocious and later heifers (PHG = 18 &#177; 1 vs. PLG = 29 &#177; 1 months; LHG = 24 &#177; 1 vs. LLG = 34 &#177; 1 months of age). The EPD to age at first calving was the main factor affecting the age at puberty. However, the ADG was limiting to puberty onset. The objective of experiment II was to evaluate the effect of metabolic imprinting from 3 to 7 months of age on puberty attainment of crossbreed heifers (Angus x Nellore). The treatments were arranged in 2 x 2 factorial design, where the factor 1 was high (H) and medium (M) ADG from 3 to 7 months of age (phase 1) and the factor 2 was high and medium ADG from 7 months of age to puberty onset (phase 2), resulting in the following treatments: CHH crossbreed heifers submitted to high ADG in both phases of experiment; CHM high ADG in phase 1 and medium ADG in phase 2; CMH medium ADG in phase 1 and high ADG in phase 2; CMM Medium ADG in both phases. The medium ADG were targeted by restricting of dry mater intake (DMI) in medium ADG. Crossbreed heifers of treatments CHH, CHM, CMH showed the same age at puberty, about 12 months. Heifers submitted to high ADG on phase 2 were heavier (P = 0,0379) at puberty than heifers submitted to low ADG. The high ADG from 3 to 7 months did not affect puberty onset in crossbreed heifers. The objective and methodology used in experiment III was the same of used in experiment II. However, Nellore heifers (N) were used instead of crossbreed heifers and the experimental period ended at 19 months of age. The NHH treatment (84%) induced higher (P = 0,0145) percentage of pubertal heifers than NMM (23%), but there was not difference in puberty rate between NHM (60%) and NMH (50%) treatments. Furthermore, the comportment of curves of puberty of treatments NHM and NMH were similar, thus there was not effect of metabolic imprinting in Nellore heifers. The high ADG from 3 to 19 months of age increased the percentage of pubertal Nellore heifers at 19 months of age

Doctor of Philosophy / Department of Animal Sciences and Industry / Michael E. Dikeman / Two experiments were conducted to evaluate the effects of dietary vitamin A on growth, carcass characteristics, and meat quality of ruminants. In Experiment 1, 40 crossbred wethers (BW = 28.7 kg) were assigned to 1 of 4 treatments: backgrounding (BG) and finishing (FN) with no vitamin A (LL); BG with no vitamin A, FN with high vitamin A (6,600 IU[dot in middle of line]kg [superscript-1] diet) (LH); BG with high vitamin A and FN with no vitamin A (HL); and BG and FN with high vitamin A (HH). During BG (d 1 to 56), intake was restricted to achieve 0.22 kg ADG. During FN (d 57 to 112), lambs consumed the same diet ad libitum. Lambs were humanely slaughtered after 112 d. There were no treatment differences (P > 0.05) in feed intake, ADG, or final BW. Carcasses from the HH group had higher (P < .05) marbling scores (514 vs. 459), and 25.8 % more extractable intramuscular lipid (IMF) than LL (3.88 vs. 3.08 % for HH and LL, respectively, P < .05); the LH and HL treatments were intermediate. The was a negative correlation (r = -0.38) between serum fatty acid content and %IMF. Experiment 1 data suggest that increased marbling may be achieved with high vitamin A for 112 d in lambs. In Experiment 2, Angus crossbred steers (n = 48), were either early-weaned (EW) at 137[plus or minus]26 d of age or weaned at a traditional age (TW) 199[plus or minus]26 d and allotted to either 42,180 IU vitamin A[dot in middle of line]hd[superscript-1][dot in middle of line]d[superscript-1] (HA) or no vitamin A (NA). Early- and TW steers consumed treatments for 235[plus or minus]17 and 175[plus or minus]18 d, respectively. Serum and liver retinol content diverged dramatically (both, P < 0.01) by the end of the experiment and TW steers tended (P > 0.10) to have higher ADG than EW steers (1.31[plus or minus]0.2 and 1.48[plus or minus]0.2 kg[dot in middle of line]hd[superscript-1][dot in middle of line]d[superscript-1], respectively). Steers were humanely slaughtered at 1.02 cm fat. Weights tended (P = 0.08) to be heavier and carcasses were fatter (P < 0.05) for HA than NA. Marbling score and % IMF were higher (P < 0.05) for EW-NA than other treatments. Percentage of USDA Choice and Prime carcasses doubled (P < 0.05) for NA than HA. Yield grades increased (P < 0.05) with EW-HA and were similar (P > 0.10) among other treatments. Feeding NA was effective for increasing marbling without increasing fat; EW enhanced these effects. Reasons for the contradictory results in these 2 experiments are unclear. Species differences in the ability to metabolize retinol are implicated.

Investigamos a distribuição de ghrelina e de seu receptor (GHS-R) na mucosa gástrica de ratos durante a terceira semana de vida pós-natal e avaliamos o efeito do desmame precoce sobre estas moléculas. Estudamos também a participação da ghrelina no controle da proliferação celular do epitélio gástrico, e para tanto utilizamos a administração de um antagonista. Detectamos o aumento do número de células imunomarcadas para ghrelina nos animais desmamados precocemente e observamos que nem a expressão de GHS-R nem a concentração proteica deste receptor foram alteradas pela mudança da dieta. O uso do antagonista [D-Lys-3]-GHRP-6 resultou na diminuição do índice de síntese de DNA no epitélio gástrico. Concluímos que a ghrelina e o GHS-R estão distribuídos no estômago durante a terceira semana de vida pós-natal e que o desmame precoce aumenta os níveis de ghrelina no epitélio gástrico, sem comprometer seu receptor. Por fim, sugerimos que esta modulação pode estar envolvida no controle da proliferação celular que é fundamental para o desenvolvimento do estômago. / In the present study, we investigated the distribution of ghrelin and growth hormone secretagogue receptor (GHS-R) in the rat gastric mucosa during the third postnatal week, and evaluated the effects of early weaning on these molecules. In addition, we studied whether ghrelin is part of cell proliferation control in gastric epithelium, and to that we used an antagonist. We detected an increase of ghrelin immunolabelled cells in animals submitted to early weaning and observed that GHS-R expression and protein levels of this receptor were not altered by dietary change. The antagonist [D-Lys-3]-GHRP-6 reduced DNA synthesis index. We concluded that ghrelin and GHS-R are distributed in the gastric mucosa during the third postnatal week and that early weaning increases hormone levels in the gastric epithelium, without changing its receptor. We can suggest that such modulation might be involved in the control of cell proliferation, which is essential for stomach development.

No description available.