{"id":{"repo_id":"dialnet","oai_identifier":"oai:dialnet.unirioja.es:TES0000023188"},"canonical_url":"https://search.dev.ndltd.org/etd/dialnet/oai:dialnet.unirioja.es:TES0000023188","repository":{"repo_id":"dialnet","name":"Dialnet","base_url":"https://dialnet.unirioja.es/oaites/OAIHandler"},"display":{"title":"Composición de la microbiota en pacientes pediátricos con déficit de hormona de crecimiento antes y después de recibir tratamiento con hormona de crecimiento","abstract":"The microbiota is defined as the community of micro-organisms that inhabit a specific environment. Generally, commensal microorganisms populate all epithelial surfaces of the body, the most numerous and complex being the gut. Alterations in the composition and functionality of the microbiota (dysbiosis) have been associated with various pathologies. Among the different functions of the microbiota, its role in growth is particularly important. Indeed, several studies have shown that germ-free mice lacking gut microbiota have reduced levels of insulin-like growth factor-1 (IGF-1) and insulin-like growth factor transporter protein-3 (IGFBP-3) and poor growth, with decreased linear growth and body weight, suggesting that mammals require the gut microbiota to ensure optimal growth. In this regard, studies in preclinical animal models have shown that physiological levels of growth hormone (GH) maintain gut integrity and improve digestive function. This effect of GH occurs synergistically with IGF-1, as observed in bone growth, metabolic and intestinal homeostasis, suggesting some association between the GH-IGF-1 axis and the gut microbiota. GH deficiency in children has a prevalence of 1:3,480 children, and can occur in isolation or associated to other pituitary deficits. Clinically it is characterised by harmonic and postnatal hypogrowth. They have a decreased response to stimulation tests and reduced levels of IGF-1 and IGFBP-3. The indicated treatment is recombinant human GH. Therefore, and given the analytical characteristics of these patients, with decreased GH and IGF-1 levels, the aim of the present study was to investigate whether these alterations were associated with changes in intestinal physiology/integrity as well as in the intestinal microbiota composition. To achieve this objective, a case-control study was performed in 21 patients with GH deficiency prior to baseline and after 6 months of GH treatment and in 20 healthy controls. Anthropometric data, analytical data, markers of inflammation, bacterial translocation and also the composition of the microbiome was determined by massive sequencing of the 16S rRNA gene, with comparison between cases and controls. The same data were analysed in patients with GH deficiency after treatment with growth hormone. Our results showed that patients with GH deficiency had lower height and lower IGF-1 and IGFBP-3 levels than controls, with a significant increase in both parameters after starting treatment. A disturbance was also observed in the two bacterial translocation markers studied, LBP and sCD14, with statistically significant differences in the latter. Our study shows that after GH treatment there is a significant increase in IGF-1 and IGFBP-3 levels in parallel with the observed reduction in bacterial translocation, underlining the bidirectional association between IGF-1-GH and gut/microbiota functionality. But it is also important to relate this improvement in TB after GH treatment to the significant decrease observed in faecal calprotectin levels after GH treatment, which underlines that GH administration is improving not only gut functionality and architecture but also gut inflammation, at a local level. No significant differences in the composition, α- or β-diversity of the gut microbiota were visualised between cases and controls, and no differences were observed in GH-deficient patients after treatment. To our knowledge, this is one of the first studies to compare the levels of bacterial translocation in children with ‘short stature’ and growth hormone deficiency with healthy controls, and also to study possible changes after GH treatment, which supports the interest of this work. In this regard, the increase observed in bacterial translocation in GH-deficient children, which is restored after GH treatment, is very interesting. In conclusion, our work demonstrates that a growth hormone deficiency (pathological hypocrectile growth and two GH stimulation tests with a low response < 7 ng/mL) in children is not accompanied by changes in the composition of the gut microbiota compared to the microbiota of healthy children, nor is it modified after treatment for 6 months with GH. However, this growth deficit and low levels of IGF-1 and GH were associated with an increase in bacterial translocation, which was reversed after treatment and with a decrease in gut inflammation, underlining the beneficial role of GH and IGF-1, not only at the level of growth, but also of gut integrity and thus of all gut-related axes: gut-brain, gut-liver axis, etc. Further studies (with prolonged periods of treatment, or with more severe GH deficits) are needed to understand in detail the association between GH-IGF-1 and gut and its impact on children's health, both in the short and long term.","abstract_html":"The microbiota is defined as the community of micro-organisms that inhabit a specific environment. Generally, commensal microorganisms populate all epithelial surfaces of the body, the most numerous and complex being the gut. Alterations in the composition and functionality of the microbiota (dysbiosis) have been associated with various pathologies. Among the different functions of the microbiota, its role in growth is particularly important. Indeed, several studies have shown that germ-free mice lacking gut microbiota have reduced levels of insulin-like growth factor-1 (IGF-1) and insulin-like growth factor transporter protein-3 (IGFBP-3) and poor growth, with decreased linear growth and body weight, suggesting that mammals require the gut microbiota to ensure optimal growth. In this regard, studies in preclinical animal models have shown that physiological levels of growth hormone (GH) maintain gut integrity and improve digestive function. This effect of GH occurs synergistically with IGF-1, as observed in bone growth, metabolic and intestinal homeostasis, suggesting some association between the GH-IGF-1 axis and the gut microbiota. GH deficiency in children has a prevalence of 1:3,480 children, and can occur in isolation or associated to other pituitary deficits. Clinically it is characterised by harmonic and postnatal hypogrowth. They have a decreased response to stimulation tests and reduced levels of IGF-1 and IGFBP-3. The indicated treatment is recombinant human GH. Therefore, and given the analytical characteristics of these patients, with decreased GH and IGF-1 levels, the aim of the present study was to investigate whether these alterations were associated with changes in intestinal physiology/integrity as well as in the intestinal microbiota composition. To achieve this objective, a case-control study was performed in 21 patients with GH deficiency prior to baseline and after 6 months of GH treatment and in 20 healthy controls. Anthropometric data, analytical data, markers of inflammation, bacterial translocation and also the composition of the microbiome was determined by massive sequencing of the 16S rRNA gene, with comparison between cases and controls. The same data were analysed in patients with GH deficiency after treatment with growth hormone. Our results showed that patients with GH deficiency had lower height and lower IGF-1 and IGFBP-3 levels than controls, with a significant increase in both parameters after starting treatment. A disturbance was also observed in the two bacterial translocation markers studied, LBP and sCD14, with statistically significant differences in the latter. Our study shows that after GH treatment there is a significant increase in IGF-1 and IGFBP-3 levels in parallel with the observed reduction in bacterial translocation, underlining the bidirectional association between IGF-1-GH and gut/microbiota functionality. But it is also important to relate this improvement in TB after GH treatment to the significant decrease observed in faecal calprotectin levels after GH treatment, which underlines that GH administration is improving not only gut functionality and architecture but also gut inflammation, at a local level. No significant differences in the composition, α- or β-diversity of the gut microbiota were visualised between cases and controls, and no differences were observed in GH-deficient patients after treatment. To our knowledge, this is one of the first studies to compare the levels of bacterial translocation in children with ‘short stature’ and growth hormone deficiency with healthy controls, and also to study possible changes after GH treatment, which supports the interest of this work. In this regard, the increase observed in bacterial translocation in GH-deficient children, which is restored after GH treatment, is very interesting. In conclusion, our work demonstrates that a growth hormone deficiency (pathological hypocrectile growth and two GH stimulation tests with a low response &lt; 7 ng/mL) in children is not accompanied by changes in the composition of the gut microbiota compared to the microbiota of healthy children, nor is it modified after treatment for 6 months with GH. However, this growth deficit and low levels of IGF-1 and GH were associated with an increase in bacterial translocation, which was reversed after treatment and with a decrease in gut inflammation, underlining the beneficial role of GH and IGF-1, not only at the level of growth, but also of gut integrity and thus of all gut-related axes: gut-brain, gut-liver axis, etc. Further studies (with prolonged periods of treatment, or with more severe GH deficits) are needed to understand in detail the association between GH-IGF-1 and gut and its impact on children&#x27;s health, both in the short and long term.","abstract_has_math":false,"creators":["García Navas, Patricia"],"institution":"Universidad de La Rioja (España)","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Pérez Matute, Patricia (Universidad de La Rioja)","Ruiz del Prado, Mª Yolanda (Universidad de La Rioja)"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2025,"date_issued":"2025","date_published":"2025","updated_at":"2026-07-24T06:27:07Z","subjects":[],"languages":["spa"],"rights":["LICENCIA DE USO: Los documentos a texto completo incluidos en Dialnet son de acceso libre y propiedad de sus autores y/o editores. Por tanto, cualquier acto de reproducción, distribución, comunicación pública y/o transformación total o parcial requiere el consentimiento expreso y escrito de aquéllos. Cualquier enlace al texto completo de estos documentos deberá hacerse a través de la URL oficial de éstos en Dialnet. Más información: https://dialnet.unirioja.es/info/derechosOAI | INTELLECTUAL PROPERTY RIGHTS STATEMENT: Full text documents hosted by Dialnet are protected by copyright and/or related rights. This digital object is accessible without charge, but its use is subject to the licensing conditions set by its authors or editors. Unless expressly stated otherwise in the licensing conditions, you are free to linking, browsing, printing and making a copy for your own personal purposes. All other acts of reproduction and communication to the public are subject to the licensing conditions expressed by editors and authors and require consent from them. Any link to this document should be made using its official URL in Dialnet. More info: https://dialnet.unirioja.es/info/derechosOAI"],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://dialnet.unirioja.es/servlet/oaites?codigo=385801","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Pérez Matute, Patricia (Universidad de La Rioja)","Ruiz del Prado, Mª Yolanda (Universidad de La Rioja)"]},{"key":"dc:creator","label":"Author","values":["García Navas, Patricia"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2025"]},{"key":"dc:publisher","label":"Institution","values":["Universidad de La Rioja (España)"]},{"key":"dc:type","label":"Dc Type","values":["text (thesis)"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["spa"]},{"key":"dc:rights","label":"Dc Rights","values":["LICENCIA DE USO: Los documentos a texto completo incluidos en Dialnet son de acceso libre y propiedad de sus autores y/o editores. Por tanto, cualquier acto de reproducción, distribución, comunicación pública y/o transformación total o parcial requiere el consentimiento expreso y escrito de aquéllos. Cualquier enlace al texto completo de estos documentos deberá hacerse a través de la URL oficial de éstos en Dialnet. Más información: https://dialnet.unirioja.es/info/derechosOAI | INTELLECTUAL PROPERTY RIGHTS STATEMENT: Full text documents hosted by Dialnet are protected by copyright and/or related rights. This digital object is accessible without charge, but its use is subject to the licensing conditions set by its authors or editors. Unless expressly stated otherwise in the licensing conditions, you are free to linking, browsing, printing and making a copy for your own personal purposes. All other acts of reproduction and communication to the public are subject to the licensing conditions expressed by editors and authors and require consent from them. Any link to this document should be made using its official URL in Dialnet. More info: https://dialnet.unirioja.es/info/derechosOAI"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://dialnet.unirioja.es/servlet/oaites?codigo=385801"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["The microbiota is defined as the community of micro-organisms that inhabit a specific environment. Generally, commensal microorganisms populate all epithelial surfaces of the body, the most numerous and complex being the gut. Alterations in the composition and functionality of the microbiota (dysbiosis) have been associated with various pathologies. Among the different functions of the microbiota, its role in growth is particularly important. Indeed, several studies have shown that germ-free mice lacking gut microbiota have reduced levels of insulin-like growth factor-1 (IGF-1) and insulin-like growth factor transporter protein-3 (IGFBP-3) and poor growth, with decreased linear growth and body weight, suggesting that mammals require the gut microbiota to ensure optimal growth. In this regard, studies in preclinical animal models have shown that physiological levels of growth hormone (GH) maintain gut integrity and improve digestive function. This effect of GH occurs synergistically with IGF-1, as observed in bone growth, metabolic and intestinal homeostasis, suggesting some association between the GH-IGF-1 axis and the gut microbiota. GH deficiency in children has a prevalence of 1:3,480 children, and can occur in isolation or associated to other pituitary deficits. Clinically it is characterised by harmonic and postnatal hypogrowth. They have a decreased response to stimulation tests and reduced levels of IGF-1 and IGFBP-3. The indicated treatment is recombinant human GH. Therefore, and given the analytical characteristics of these patients, with decreased GH and IGF-1 levels, the aim of the present study was to investigate whether these alterations were associated with changes in intestinal physiology/integrity as well as in the intestinal microbiota composition. To achieve this objective, a case-control study was performed in 21 patients with GH deficiency prior to baseline and after 6 months of GH treatment and in 20 healthy controls. Anthropometric data, analytical data, markers of inflammation, bacterial translocation and also the composition of the microbiome was determined by massive sequencing of the 16S rRNA gene, with comparison between cases and controls. The same data were analysed in patients with GH deficiency after treatment with growth hormone. Our results showed that patients with GH deficiency had lower height and lower IGF-1 and IGFBP-3 levels than controls, with a significant increase in both parameters after starting treatment. A disturbance was also observed in the two bacterial translocation markers studied, LBP and sCD14, with statistically significant differences in the latter. Our study shows that after GH treatment there is a significant increase in IGF-1 and IGFBP-3 levels in parallel with the observed reduction in bacterial translocation, underlining the bidirectional association between IGF-1-GH and gut/microbiota functionality. But it is also important to relate this improvement in TB after GH treatment to the significant decrease observed in faecal calprotectin levels after GH treatment, which underlines that GH administration is improving not only gut functionality and architecture but also gut inflammation, at a local level. No significant differences in the composition, α- or β-diversity of the gut microbiota were visualised between cases and controls, and no differences were observed in GH-deficient patients after treatment. To our knowledge, this is one of the first studies to compare the levels of bacterial translocation in children with ‘short stature’ and growth hormone deficiency with healthy controls, and also to study possible changes after GH treatment, which supports the interest of this work. In this regard, the increase observed in bacterial translocation in GH-deficient children, which is restored after GH treatment, is very interesting. In conclusion, our work demonstrates that a growth hormone deficiency (pathological hypocrectile growth and two GH stimulation tests with a low response < 7 ng/mL) in children is not accompanied by changes in the composition of the gut microbiota compared to the microbiota of healthy children, nor is it modified after treatment for 6 months with GH. However, this growth deficit and low levels of IGF-1 and GH were associated with an increase in bacterial translocation, which was reversed after treatment and with a decrease in gut inflammation, underlining the beneficial role of GH and IGF-1, not only at the level of growth, but also of gut integrity and thus of all gut-related axes: gut-brain, gut-liver axis, etc. Further studies (with prolonged periods of treatment, or with more severe GH deficits) are needed to understand in detail the association between GH-IGF-1 and gut and its impact on children's health, both in the short and long term.","La microbiota se define como la comunidad de microorganismos que habitan en un ambiente específico. En general, los microorganismos comensales pueblan todas las superficies epiteliales del cuerpo, siendo el más numeroso y complejo el intestinal. Alteraciones en la composición y funcionalidad de la microbiota (disbiosis) se han asociado con diversas patologías. Entre las diferentes funciones que ejerce la microbiota, cabe destacar su papel en el crecimiento. De hecho, varios estudios han demostrado que los ratones libres de gérmenes, que carecen de microbiota intestinal, presentan unos niveles de factor de crecimiento similar a la insulina 1 (IGF-1) y de proteína transportadora 3 del factor de crecimiento similar a la insulina (IGFBP-3) reducidos y tienen un crecimiento deficiente, con una disminución del crecimiento lineal y del peso corporal, lo que sugiere que los mamíferos requieren la microbiota intestinal para garantizar un crecimiento óptimo. En este sentido, estudios en modelos preclínicos de animales han demostrado que los niveles fisiológicos de hormona de crecimiento (GH) mantienen la integridad intestinal y mejoran la función digestiva. Este efecto de la GH ocurre de manera sinérgica con el IGF-1, como se observa en el crecimiento óseo, metabólico y la homeostasis intestinal sugiriendo algún tipo de asociación entre el eje GH-IGF-1 y la microbiota intestinal. El déficit de GH en niños tiene una prevalencia de 1:3.480 niños, y se puede dar de manera aislada o asociada a otros déficits hipofisarios. Clínicamente se caracteriza por un hipocrecimiento armónico y postnatal. Presentan una respuesta disminuida a los test de estímulo y unos niveles reducidos de IGF-1 e IGFBP-3. El tratamiento indicado es GH humana recombinante. Por todo ello, y dadas las características analíticas de estos pacientes, con niveles de GH e IGF-1 disminuidos, el objetivo del presente trabajo fue investigar si dichas alteraciones se asociaban con cambios en la fisiología/integridad intestinal así como en la composición de la microbiota intestinal. Para lograr este objetivo se realizó un estudio de casos y controles en 21 pacientes con déficit de GH previo al inicio y tras 6 meses de tratamiento con GH y en 20 controles sanos. Se estudiaron los datos antropométricos, analíticos, marcadores de inflamación, de translocación bacteriana y también se determinó la composición del microbioma mediante secuenciación masiva del gen del ARNr 16S, realizándose la comparación 28 entre casos y controles. Se analizaron estos mismos datos en los pacientes con déficit de GH tras recibir tratamiento con hormona de crecimiento. Nuestros resultados mostraron que los pacientes con déficit de GH presentaron una talla y unas cifras de IGF-1 e IGFBP-3 menores que los controles, produciéndose un aumento de ambos parámetros de manera significativa tras iniciar el tratamiento. Se observó también una alteración en los dos marcadores de translocación bacteriana estudiados, LBP y sCD14, alcanzándose en este último diferencias estadísticamente significativas. Nuestro estudio demuestra que tras el tratamiento con GH se produce un incremento significativo en los niveles de IGF-1 e IGFBP-3 en paralelo con la reducción observada en la translocación bacteriana lo que subraya esa asociación bidireccional entre IGF-1-GH y la funcionalidad del intestino/microbiota. Pero, además, es importante relacionar esta mejoría en la TB tras el tratamiento con GH con la disminución significativa observada en los niveles de calprotectina fecal tras dicho tratamiento, lo que subraya que la administración de GH está mejorando no sólo la funcionalidad y arquitectura intestinal si no también la inflamación intestinal, a nivel local. No se visualizaron diferencias significativas en la composición, ni en la ɲ o la ɴ diversidad de la microbiota intestinal entre los casos y los controles, y tampoco se observaron diferencias en los pacientes con déficit de GH tras el tratamiento. Según nuestro conocimiento, éste es uno de los primeros estudios en el que se han comparado los niveles de translocación bacteriana en niños con «talla baja» y con déficit de hormona de crecimiento respecto a controles sanos, y también en el que se han estudiado los posibles cambios tras el tratamiento con GH, lo cual refrenda el interés de este trabajo. En este sentido, es muy interesante el incremento observado en la translocación bacteriana en los niños con déficit de GH que se restituye tras el tratamiento con GH. En conclusión, nuestro trabajo demuestra que un déficit de hormona de crecimiento (hipocrecimiento patológico y dos test de estímulo de GH con una respuesta escasa < 7 ng/mL) en niños no se acompaña de cambios en la composición de la microbiota intestinal en comparación con la microbiota de niños sanos, ni tampoco se ve modificada tras el tratamiento durante 6 meses con GH. Sin embargo, este déficit de 29 crecimiento y niveles bajos de IGF-1 y GH si se asoció con un incremento en la trasloca."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Composición de la microbiota en pacientes pediátricos con déficit de hormona de crecimiento antes y después de recibir tratamiento con hormona de crecimiento"]}]}],"canonical_facts":{"dc:contributor":["Pérez Matute, Patricia (Universidad de La Rioja)","Ruiz del Prado, Mª Yolanda (Universidad de La Rioja)"],"dc:creator":["García Navas, Patricia"],"dc:date":["2025"],"dc:description":["The microbiota is defined as the community of micro-organisms that inhabit a specific environment. Generally, commensal microorganisms populate all epithelial surfaces of the body, the most numerous and complex being the gut. Alterations in the composition and functionality of the microbiota (dysbiosis) have been associated with various pathologies. Among the different functions of the microbiota, its role in growth is particularly important. Indeed, several studies have shown that germ-free mice lacking gut microbiota have reduced levels of insulin-like growth factor-1 (IGF-1) and insulin-like growth factor transporter protein-3 (IGFBP-3) and poor growth, with decreased linear growth and body weight, suggesting that mammals require the gut microbiota to ensure optimal growth. In this regard, studies in preclinical animal models have shown that physiological levels of growth hormone (GH) maintain gut integrity and improve digestive function. This effect of GH occurs synergistically with IGF-1, as observed in bone growth, metabolic and intestinal homeostasis, suggesting some association between the GH-IGF-1 axis and the gut microbiota. GH deficiency in children has a prevalence of 1:3,480 children, and can occur in isolation or associated to other pituitary deficits. Clinically it is characterised by harmonic and postnatal hypogrowth. They have a decreased response to stimulation tests and reduced levels of IGF-1 and IGFBP-3. The indicated treatment is recombinant human GH. Therefore, and given the analytical characteristics of these patients, with decreased GH and IGF-1 levels, the aim of the present study was to investigate whether these alterations were associated with changes in intestinal physiology/integrity as well as in the intestinal microbiota composition. To achieve this objective, a case-control study was performed in 21 patients with GH deficiency prior to baseline and after 6 months of GH treatment and in 20 healthy controls. Anthropometric data, analytical data, markers of inflammation, bacterial translocation and also the composition of the microbiome was determined by massive sequencing of the 16S rRNA gene, with comparison between cases and controls. The same data were analysed in patients with GH deficiency after treatment with growth hormone. Our results showed that patients with GH deficiency had lower height and lower IGF-1 and IGFBP-3 levels than controls, with a significant increase in both parameters after starting treatment. A disturbance was also observed in the two bacterial translocation markers studied, LBP and sCD14, with statistically significant differences in the latter. Our study shows that after GH treatment there is a significant increase in IGF-1 and IGFBP-3 levels in parallel with the observed reduction in bacterial translocation, underlining the bidirectional association between IGF-1-GH and gut/microbiota functionality. But it is also important to relate this improvement in TB after GH treatment to the significant decrease observed in faecal calprotectin levels after GH treatment, which underlines that GH administration is improving not only gut functionality and architecture but also gut inflammation, at a local level. No significant differences in the composition, α- or β-diversity of the gut microbiota were visualised between cases and controls, and no differences were observed in GH-deficient patients after treatment. To our knowledge, this is one of the first studies to compare the levels of bacterial translocation in children with ‘short stature’ and growth hormone deficiency with healthy controls, and also to study possible changes after GH treatment, which supports the interest of this work. In this regard, the increase observed in bacterial translocation in GH-deficient children, which is restored after GH treatment, is very interesting. In conclusion, our work demonstrates that a growth hormone deficiency (pathological hypocrectile growth and two GH stimulation tests with a low response < 7 ng/mL) in children is not accompanied by changes in the composition of the gut microbiota compared to the microbiota of healthy children, nor is it modified after treatment for 6 months with GH. However, this growth deficit and low levels of IGF-1 and GH were associated with an increase in bacterial translocation, which was reversed after treatment and with a decrease in gut inflammation, underlining the beneficial role of GH and IGF-1, not only at the level of growth, but also of gut integrity and thus of all gut-related axes: gut-brain, gut-liver axis, etc. Further studies (with prolonged periods of treatment, or with more severe GH deficits) are needed to understand in detail the association between GH-IGF-1 and gut and its impact on children's health, both in the short and long term.","La microbiota se define como la comunidad de microorganismos que habitan en un ambiente específico. En general, los microorganismos comensales pueblan todas las superficies epiteliales del cuerpo, siendo el más numeroso y complejo el intestinal. Alteraciones en la composición y funcionalidad de la microbiota (disbiosis) se han asociado con diversas patologías. Entre las diferentes funciones que ejerce la microbiota, cabe destacar su papel en el crecimiento. De hecho, varios estudios han demostrado que los ratones libres de gérmenes, que carecen de microbiota intestinal, presentan unos niveles de factor de crecimiento similar a la insulina 1 (IGF-1) y de proteína transportadora 3 del factor de crecimiento similar a la insulina (IGFBP-3) reducidos y tienen un crecimiento deficiente, con una disminución del crecimiento lineal y del peso corporal, lo que sugiere que los mamíferos requieren la microbiota intestinal para garantizar un crecimiento óptimo. En este sentido, estudios en modelos preclínicos de animales han demostrado que los niveles fisiológicos de hormona de crecimiento (GH) mantienen la integridad intestinal y mejoran la función digestiva. Este efecto de la GH ocurre de manera sinérgica con el IGF-1, como se observa en el crecimiento óseo, metabólico y la homeostasis intestinal sugiriendo algún tipo de asociación entre el eje GH-IGF-1 y la microbiota intestinal. El déficit de GH en niños tiene una prevalencia de 1:3.480 niños, y se puede dar de manera aislada o asociada a otros déficits hipofisarios. Clínicamente se caracteriza por un hipocrecimiento armónico y postnatal. Presentan una respuesta disminuida a los test de estímulo y unos niveles reducidos de IGF-1 e IGFBP-3. El tratamiento indicado es GH humana recombinante. Por todo ello, y dadas las características analíticas de estos pacientes, con niveles de GH e IGF-1 disminuidos, el objetivo del presente trabajo fue investigar si dichas alteraciones se asociaban con cambios en la fisiología/integridad intestinal así como en la composición de la microbiota intestinal. Para lograr este objetivo se realizó un estudio de casos y controles en 21 pacientes con déficit de GH previo al inicio y tras 6 meses de tratamiento con GH y en 20 controles sanos. Se estudiaron los datos antropométricos, analíticos, marcadores de inflamación, de translocación bacteriana y también se determinó la composición del microbioma mediante secuenciación masiva del gen del ARNr 16S, realizándose la comparación 28 entre casos y controles. Se analizaron estos mismos datos en los pacientes con déficit de GH tras recibir tratamiento con hormona de crecimiento. Nuestros resultados mostraron que los pacientes con déficit de GH presentaron una talla y unas cifras de IGF-1 e IGFBP-3 menores que los controles, produciéndose un aumento de ambos parámetros de manera significativa tras iniciar el tratamiento. Se observó también una alteración en los dos marcadores de translocación bacteriana estudiados, LBP y sCD14, alcanzándose en este último diferencias estadísticamente significativas. Nuestro estudio demuestra que tras el tratamiento con GH se produce un incremento significativo en los niveles de IGF-1 e IGFBP-3 en paralelo con la reducción observada en la translocación bacteriana lo que subraya esa asociación bidireccional entre IGF-1-GH y la funcionalidad del intestino/microbiota. Pero, además, es importante relacionar esta mejoría en la TB tras el tratamiento con GH con la disminución significativa observada en los niveles de calprotectina fecal tras dicho tratamiento, lo que subraya que la administración de GH está mejorando no sólo la funcionalidad y arquitectura intestinal si no también la inflamación intestinal, a nivel local. No se visualizaron diferencias significativas en la composición, ni en la ɲ o la ɴ diversidad de la microbiota intestinal entre los casos y los controles, y tampoco se observaron diferencias en los pacientes con déficit de GH tras el tratamiento. Según nuestro conocimiento, éste es uno de los primeros estudios en el que se han comparado los niveles de translocación bacteriana en niños con «talla baja» y con déficit de hormona de crecimiento respecto a controles sanos, y también en el que se han estudiado los posibles cambios tras el tratamiento con GH, lo cual refrenda el interés de este trabajo. En este sentido, es muy interesante el incremento observado en la translocación bacteriana en los niños con déficit de GH que se restituye tras el tratamiento con GH. En conclusión, nuestro trabajo demuestra que un déficit de hormona de crecimiento (hipocrecimiento patológico y dos test de estímulo de GH con una respuesta escasa < 7 ng/mL) en niños no se acompaña de cambios en la composición de la microbiota intestinal en comparación con la microbiota de niños sanos, ni tampoco se ve modificada tras el tratamiento durante 6 meses con GH. Sin embargo, este déficit de 29 crecimiento y niveles bajos de IGF-1 y GH si se asoció con un incremento en la trasloca."],"dc:format":["application/pdf"],"dc:identifier":["https://dialnet.unirioja.es/servlet/oaites?codigo=385801"],"dc:language":["spa"],"dc:publisher":["Universidad de La Rioja (España)"],"dc:rights":["LICENCIA DE USO: Los documentos a texto completo incluidos en Dialnet son de acceso libre y propiedad de sus autores y/o editores. Por tanto, cualquier acto de reproducción, distribución, comunicación pública y/o transformación total o parcial requiere el consentimiento expreso y escrito de aquéllos. Cualquier enlace al texto completo de estos documentos deberá hacerse a través de la URL oficial de éstos en Dialnet. Más información: https://dialnet.unirioja.es/info/derechosOAI | INTELLECTUAL PROPERTY RIGHTS STATEMENT: Full text documents hosted by Dialnet are protected by copyright and/or related rights. This digital object is accessible without charge, but its use is subject to the licensing conditions set by its authors or editors. Unless expressly stated otherwise in the licensing conditions, you are free to linking, browsing, printing and making a copy for your own personal purposes. All other acts of reproduction and communication to the public are subject to the licensing conditions expressed by editors and authors and require consent from them. Any link to this document should be made using its official URL in Dialnet. More info: https://dialnet.unirioja.es/info/derechosOAI"],"dc:title":["Composición de la microbiota en pacientes pediátricos con déficit de hormona de crecimiento antes y después de recibir tratamiento con hormona de crecimiento"],"dc:type":["text (thesis)"]},"updated_at":"2026-07-24T06:27:07Z"}