Neglected function of gastrin to reduce feeding in Siberian sturgeon (Acipenser baerii) via cholecystokinin receptor B.

Gastrin is an important intragastrointestinal hormone, but reports on its regulation of feeding behavior in fish are still scarce. This study aimed to determine the feeding regulatory function of gastrin in sturgeon. In this study, a gastrin/cholecystokinin-like peptide was identified in the genomes of sturgeon and proved to be gastrin by evolutionary tree analysis. Tissue distribution of gastrin and its receptor, cholecystokinin receptor B (CCKRB), showed that both had high mRNA abundance in the hypothalamus and gastrointestinal tract. In the duodenum, gastrin and CCKRB mRNAs were reduced at 1 h of fasting, and both were also observed in the stomach and hypothalamus in response to changes in feeding status. Sulfated gastrin 17 is the major form of gastrin in vivo. Therefore, we investigated the effect of sulfated gastrin 17 on feeding by intraperitoneal injection into Siberian sturgeon using sulfated gastrin 17. The results showed that gastrin 17 significantly reduced the cumulative feeding of Siberian sturgeon in the short term (1, 3 and 6 h) and long term (1, 2, 3, 4, 5 and 7 days). Finally, we explored the potential mechanism of feeding inhibition after intraperitoneal injection of gastrin 17 for 7 consecutive days. The results showed that gastrin 17 treatment significantly increased the mRNA levels of anorexigenic peptides (cart, cck and pyy), while it had no significant effect on the mRNA abundance of orexigenic peptides (npy and agrp). In addition, gastrin 17 treatment significantly affected the expression of appetite signaling pathways in the hypothalamus, such that the mRNA expression of ampkα1 was significantly reduced, whereas the mRNA abundance of stat3, mtor and s6k was significantly increased. In conclusion, the present study confirmed the anorectic effect of gastrin on Siberian sturgeon.

Gastrin: a new branch of the gastropancreatic axis that can explain the effect of sleeve gastrectomy on glucose metabolism.

BACKGROUND: Among bariatric techniques, sleeve gastrectomy (SG) stands out owing to its efficiency. The role of the stomach as a secretory organ of many substances, such as gastrin, related to insulin secretion is well known. Gastrin induces insulin release in isolated pancreatic islets, limiting somatostatin-14 intraislet release, and has been associated with blood glucose level improvement in diabetic models after SG. SG involves gastric resection along the greater curvature. This study aimed to determine the role of gastrin in glucose metabolism improvement after SG with the aid of the gastrin antagonist netazepide. METHODS: In 12 sham-operated, 12 SG-operated, and 12 SG-operated/netazepide-treated Wistar rats, we compared medium- and long-term plasma insulin, oral glucose tolerance test (OGTT) results, and plasma gastrin levels. In addition, gastrin expression was assessed in the gastric remnant, and the beta-cell mass was measured. RESULTS: SG induced a medium-term elevation of the insulin response and plasma gastrin levels without modification of the OGTT results. However, long-term depletion of the insulin response with elevated OGTT areas under the curve and plasma gastrin levels appeared after SG. Netazepide prevented the SG effect on these parameters. Gastrin tissue expression was greater in SG animals than in SG/netazepide-treated or control animals. The beta-cell mass was lower in the SG group than in the control or SG/netazepide group. CONCLUSION: Gastrin plays a central role in glucose improvement after SG. It stimulates a medium-term strong insulin response but also causes long-term beta-cell mass depletion and a loss of insulin response. These effects are prevented by gastrin antagonists such as netazepide.

Long-Term Administration of Omeprazole-Induced Hypergastrinemia and Changed Glucose Homeostasis and Expression of Metabolism-Related Genes.

Introduction: PPIs, or proton pump inhibitors, are the most widely prescribed drugs. There is a debate regarding the relationship between long-term PPI use and the risk of type 2 diabetes mellitus (T2DM). A potential connection between T2DM and PPIs could be an elevated gastrin concentration. This study is aimed at investigating the long-term effects of PPI omeprazole (OZ) on glucose homeostasis and pancreatic gene expression profile in mice. Methods: Healthy adult male BALB/c mice were randomly divided into three equal groups (n = 10 in each one): (1) experimental mice that received OZ 20 mg/kg; (2) control mice that received 30 µl saline per os; (3) intact mice without any interventions. Mice were treated for 30 weeks. Glucose homeostasis was investigated by fasting blood glucose level, oral glucose tolerance test (GTT), insulin tolerance test (ITT), and basal insulin resistance (HOMA-IR). Serum gastrin and insulin concentration were determined by ELISA. Expressions of Sirt1, Pparg, Nfκb1 (p105), Nfe2l2, Cxcl5, Smad3, H2a.z, and H3f3b were measured by RT-PCR. Result: The ROC analysis revealed an increase in fasting blood glucose levels in OZ-treated mice in comparison with control and intact groups during the 30-week experiment. A slight but statistically significant increase in glucose tolerance and insulin sensitivity was observed in OZ-treated mice within 30 weeks of the experiment. The mice treated with OZ exhibited significant increases in serum insulin and gastrin levels, accompanied by a rise in the HOMA-IR level. These animals had a statistically significant increase in Sirt1, Pparg, and Cxcl5 mRNA expression. There were no differences in ß-cell numbers between groups. Conclusion: Long-term OZ treatment induced hypergastrin- and hyperinsulinemia and increased expression of Sirt1, Pparg, and Cxcl5 in mouse pancreatic tissues accompanied by specific changes in glucose metabolism. The mechanism of omeprazole-induced Cxcl5 mRNA expression and its association with pancreatic cancer risk should be investigated.

Over-expression of gastrin inhibits apoptosis of gastric cancer cells via reactive oxygen species and annexin A2-mediated mitochondrial dysfunction / La sobreexpresión de gastrina inhibe la apoptosis de las células de cáncer gástrico a través de especies reactivas de oxígeno y disfunción mitocondrial mediada por anexina A2

SUMMARY: Gastrin plays a vital role in the development and progression of gastric cancer (GC). Its expression is up-regulated in GC tissues and several GC cell lines. Yet, the underlying mechanism remains to be investigated. Here, we aim to investigate the role and mechanism of gastrin in GC proliferation. Gastrin-overexpressing GC cell model was constructed using SGC7901 cells. Then the differentially expressed proteins were identified by iTRAQ analysis. Next, we use flow cytometry and immunofluorescence to study the effect of gastrin on the mitochondrial potential and mitochondria-derived ROS production. Finally, we studied the underlying mechanism of gastrin regulating mitochondrial function using Co-IP, mass spectrometry and immunofluorescence. Overexpression of gastrin promoted GC cell proliferation in vitro and in vivo. A total of 173 proteins were expressed differently between the controls and gastrin- overexpression cells and most of these proteins were involved in tumorigenesis and cell proliferation. Among them, Cox17, Cox5B and ATP5J that were all localized to the mitochondrial respiratory chain were down-regulated in gastrin-overexpression cells. Furthermore, gastrin overexpression led to mitochondrial potential decrease and mitochondria-derived ROS increase. Additionally, gastrin-induced ROS generation resulted in the inhibition of cell apoptosis via activating NF-kB, inhibiting Bax expression and promoting Bcl-2 expression. Finally, we found gastrin interacted with mitochondrial membrane protein Annexin A2 using Co-IP and mass spectrometry. Overexpr ession of gastrin inhibits GC cell apoptosis by inducing mitochondrial dysfunction through interacting with mitochondrial protein Annexin A2, then up-regulating ROS production to activate NF-kB and further leading to Bax/Bcl-2 ratio decrease.

La gastrina juega un papel vital en el desarrollo y progresión del cáncer gástrico (CG). Su expresión está regulada al alza en tejidos de CG y en varias líneas celulares de CG. Sin embargo, el mecanismo subyacente aun no se ha investigado. El objetivo de este estudio fue investigar el papel y el mecanismo de la gastrina en la proliferación de CG. El modelo de células CG que sobre expresan gastrina se construyó usando células SGC7901. Luego, las proteínas expresadas diferencialmente se identificaron mediante análisis iTRAQ. A continuación, utilizamos la citometría de flujo y la inmunofluorescencia para estudiar el efecto de la gastrina en el potencial mitocondrial y la producción de ROS derivada de las mitocondrias. Finalmente, estudiamos el mecanismo subyacente de la gastrina que regula la función mitocondrial utilizando Co-IP, espectrometría de masas e inmunofluorescencia. La sobreexpresión de gastrina promovió la proliferación de células CG in vitro e in vivo. Un total de 173 proteínas se expresaron de manera diferente entre los controles y las células con sobreexpresión de gastrina y la mayoría de estas proteínas estaban implicadas en la tumorigenesis y la proliferación celular. Entre estas, Cox17, Cox5B y ATP5J, todas localizadas en la cadena respiratoria mitocondrial, estaban reguladas a la baja en las células con sobreexpresión de gastrina. Además, la sobreexpresión de gastrina provocó una disminución del potencial mitocondrial y un aumento de las ROS derivadas de las mitocondrias. Por otra parte, la generación de ROS inducida por gastrina resultó en la inhibición de la apoptosis celular mediante la activación de NF-kB, inhibiendo la expresión de Bax y promoviendo la expresión de Bcl-2. Finalmente, encontramos que la gastrina interactuaba con la proteína de membrana mitocondrial Anexina A2 usando Co-IP y espectrometría de masas. La sobreexpresión de gastrina inhibe la apoptosis de las células CG al inducir la disfunción mitocondrial a través de la interacción con la proteína mitocondrial Anexina A2, luego regula el aumento de la producción de ROS para activar NF-kB y conduce aún más a la disminución de la relación Bax/Bcl-2.

Effect of a Denture Adhesive on the Satisfaction and Kinesiographic Parameters of Complete Denture Wearers: A Cross-Over Randomized Clinical Trial

The aim of the present study was to assess the effect of a denture adhesive (DA) on patient satisfaction and kinesiographic parameters of complete denture wearers by a cross-over study. Fifty edentulous patients received a set of new complete dentures. After an adaptation period, the participants were enrolled in the trial and randomized to receive a sequence of treatment protocols: Protocol 1- DA use during the first 15 days, followed by no DA for the next 15 days; Protocol 2- no DA during the first 15 days, followed by use of DA for the next 15 days. Outcomes were assessed after 15 days of each sequence of treatment. A questionnaire was used to assess the patients´ satisfaction. A kinesiograph was used to record mandible movements and patterns of maxillary complete denture movement during chewing. The Wilcoxon test (α=0.05) and a paired sample t-test (α=0.05) were used to compare satisfaction levels and kinesiographic data, respectively. Use of DA improved the overall level of patient satisfaction (p<0.001). The kinesiographic recordings revealed a significant increase (1.7 mm) in vertical mandible movements (p<0.001) during chewing and a lower (0.3 mm) vertical intrusion of the maxillary complete dentures (p=0.002) during chewing after using the DA. Use of DA in complete denture wearers improved the patients´ satisfaction and altered mandible movements, with increases in vertical movements during chewing and less intrusion of maxillary complete dentures.

O objetivo deste estudo foi avaliar o efeito da utilização de um adesivo para prótese na satisfação e nos parâmetros cinesiográficos em usuários de próteses totais por meio de um estudo "cross-over". Cinquenta pacientes desdentados receberam novas próteses totais bimaxilares. Após um período de adaptação, os participantes incluídos no estudo receberam uma sequência de tratamento: Protocolo 1- utilização do adesivo para prótese durante os primeiros 15 dias, seguida por não utilização do adesivo os próximos 15 dias; Protocolo 2- não utilização do adesivo durante os primeiros 15 dias; seguida por utilização do adesivo nos próximos 15 dias. Os resultados foram avaliados após 15 dias de cada sequência de tratamento. Um questionário para avaliar a satisfação dos pacientes e um cinesiógrafo para registrar os movimentos mandibulares e o padrão de movimento da prótese total maxilar durante mastigação foram utilizados. O teste de "Wilcoxon" (α=0,05) e o "t-test" de Student para amostras pareadas (α=0,05) foram utilizados para comparar o grau de satisfação dos pacientes e os dados cinesiográficos, respectivamente. O adesivo para prótese melhorou significativamente a satisfação geral dos participantes (p<0,001). Os registros cinesiográficos mostraram um aumento significativo (1,7 mm) no movimento mandibular vertical (p<0,001) e uma menor intrusão (0,3 mm) da prótese total superior (p=0,002) durante a mastigação após o uso de adesivo. O uso de adesivo para prótese melhorou a satisfação dos usuários de próteses totais e gerou um aumento no movimento mandibular vertical e uma menor intrusão da prótese total maxilar durante a mastigação.

Gastrina: hormona de múltiples funciones / Gastrin: multifunctional hormone

Gastrin is a polypeptide hormone secreted primarily by G cells of the gastric antrum. Its main function is the regulation of gastric acidity, through the release of histamine, which ultimately acts on the parietal cell. There are a number of pathological conditions characterized by persistent hypergastrinemia will cause various effects, from peptic disease to cancer. Most research points to clarify their involvement in processes of proliferation of different cell types and thus to find a treatment for cancer. Intermediates molecules have been described for the metabolism of gastrin, which also possess the property of stimulating the proliferation of various cell lines and participated in processes of cell migration and invasion. Using molecular bioengineering has been able to modify the original molecule to create receptor antagonist and thus able to address some of the associated diseases. Much of this hormone, described over a century ago, is still unknown (AU)

Avances en péptidos gastrointestinales: gastrina / Advances in gastrointestinal peptides: gastrin

Péptidos gastrointestinales son el universo de hormonas verdaderas (siempre circulantes en la sangre), agentes neuro-endocrinos (liberados en la sinapsis neurales; no circulantes), substancias paracrinas (vertidas al entorno de células vecinas) y factores autocrinos (cuyo"blanco" es la misma célula generadora). La endocrinología gastrointestinal auroral ha evolucionado por edades distintas y se encuentra en plena era de "receptorología". Concecuencia natural es la actual abundancia de información procedente de tecnología complicada. Esta comunicación se propone revisar los avances en el conocimiento de gastrina que, con colecistokinina, integra una familia peptídica sobresaliente. Los temas escogidos son: a)participación en la secreción gástrica ácida; b)rteceptores en las células secretoras; c)repercución de hipergastrinemia sobre la estructura de las células enterocromafines en función de situaciones clínicas caracterizadas; d)regulación de la liberación de histamina; y e)receptores de gastrina y sus influencias sobre el epitelio colónico normal y neoplásico

Hipergastrinemia del habitante de las grandes alturas del Perú estudio comparativo con sujetos del nivel del mar / Hypergastrinemia in high altitude, natives comparative study with sea level natives

Se determinó la gastrinemia basal con técnicas de radioinmunoensayo en dos grupos homólogos de 20 varones jóvenes aparentemente sanos, uno natural y residente en Cerro de Pasco, a 4,400 m.s.n.m. y otro de Lima a 150 m.s.n.m. En el grupo de la altura se encontró una media de 113.8 +/- 55.9 pg/ml y a nivel del mar 50.2 +/- 12.3 pg/ml., con una diferencia estadísdtica altamente significativa. se plantea como posible explicación la hiperfunción secundaria o primaria de las células "G" productoras de la hormona o bién una hiperplasia de las mismas. se considera la hipergastrinemia como una peculiaridad fisiológica en el poblador de las grandes alturas y que junto con una mayor acción vagal, contribuyen a explicar por lo menos a dos factores: una mayor secreción ácida basdal y una hiporespuesta relativa a nuevos estímulos, descritos anteriormente

Lower density of antral somatostatin-immunoreactive cells in the digestive form of chronic Chagas' disease

Patients with the digestive form of chronic Chagas' disease exhibit abnormally increased gastrin release, possibly caused by antral gastrin cell (G cell) hyperfunction. In order to identify the mechanisms underlying this abnormality, we used an immunohistochemical method to assess the population of antral somatostatin-producing cells (D cells) in chagasic patients, since somatostatin is known to be the main inhibitory factor of gastrin secretion. Samples (N = 11) of endoscopic antral biopsies taken from 16 Chagas' disease patients and 13 control subjects were studied. Antral D and G cell populations were determined by an immunohistochemical technique using highly specific antibodies against somatostatin and gastrin. There was no significant difference between Chagas' disease and control groups regarding G cell population (number of cells/mm reported as median (range): 70.0 (23.7-247.0) vs 98.1 (52.7-169.4), P>0.10). In contrast, the number of antral D cells in Chagas' disease patients was significantly lower than in controls (l6.4 (6.9-54.4) vs 59.3 (29.6-113.8), P<0.05). Chronic superficial gastritis and infection with Helicobacter pylori were more frequent in chagasic patients than in controls, but there was no demonstrable association between these factors and the reduction of the number of antral D cells. These data suggest that reduction in the number of antral somatostatin-producing cells, which should lead to reduced inhibition of gastrin cell activity, may play a role in the increased gastrin secretion observed in Chagas' disease patients.

Diagnóstico y etiología del esófago de Barrett: presencia de células secretoras de gastrina (G) / Diagnosis and etiology of Barrett esophagus: presence of gastrin secreting cells (6 cells)

Presentamos las pautas diagnósticas, revisando los datos clínicos, radiológicos, endoscópicos e histológicos de 35 pacientes con Esófago de Barrett (EB) (metaplasia columnar en esófago distal). Las características clínicas son las de una esofagitis severa de larga evolución, aunque la metaplasia por sí misma, es asintomática y su clínica depende del grado de inflamación. La radiología nos revela algunos datos como reflujo GE, hernia hiatal, úlceras o estenosis, y tal vez el doble contraste haga sospechar el endobraquiesófago (EBE). La endoscopía nos proporciona datos precisos sobre la altura del EBE, úlceras, estenosis e inflamacion. La histología nos aclara el tipo de metaplasia columnar (cardial o transicional, gástrica fúndica, intestinal o especializada, ó mixta). La etiología congénita o adquirida, sujeta a controversia, puede ser aclarada con un método inmuno histoquímico, le de la Peroxidasa anti-Peroxidasa (PAP) revelándonos la presencia de células secretoras de Gastrina (G) en los casos congénitos

Alteraçöes da gastrina nas células G do antro gástrico e da gastrinemia após ressecçäo de 80% de jejunoíleo em ratos / Gastrin changes in the gastric antrum G-cell and of serum levels after 80% of jejuno ileal resection in rats

Foram estudadas as alteraçöes na populaçäo das células produtoras de gastrina do antro gástrico de ratos submetidos a ressecçäo de 80% de jejunoíleo. Aos 90 dias de pós-operatório, os animais foram mortos após 12 horas de jejum noturno para retirada do antro gástrico; visando preparaçöes histológicas específicas (método de PAP), para contagem das células G produtoras de gastrina, sendo retirado o sangue para as dosagens séricas da gastrina. Para contagem das células, utilizou-se microscopia óptica com ocular integradora histométrica de 42 pontos, tendo sido realizada a contagem em dez campos de cada corte histológico; para dosagem sérica da gastrina, utilizou-se o método de radioimunoensaio de duplo anticorpo. Os resultados obtidos evidenicaram na histometria significante diminuiçäo da populaçäo de células G com gastrina no antro dos animais enterectomizados, quando comparados ao grupo controle: neste, a percentagem média de células G encontrada fou 17,55% e, no enterectomizado, 7,99%. A dosagem sérica do hormônio mostrou significante aumento da gastrina nos animais enterectomizados, quando comparados ao controle. O valor médio da dosagem da gastrina no controle foi de 110Pg?ml e, no enterectomizado, de 170Pg/ml. Assim, o presente estudo permite concluir que, após ressecçäo de 80% de jejunoíleo, houve diminuiçäo da populçäo de células G com gastrina no antro gástrico, apesar de existir hipergastrinemia

Tumores funcionantes del páncreas

Con los avances técnicos como la microscopía electrónica, citoquímica e inmunopatología, ha sido posible identificar en los islotes de Langerhans diferentes células productoras de hormonas. Puede ocurrir hiperplasia (nesidioblastosis), formarse adenomas benignos o malignos a partir de estas células, cuya secreción hormonal no depende de estíulos fisiológicos. El tumor frecuente es el Insulinoma, que secreta insulina y el péptido C, da lugar a hipoglicemia, síntomas por respuesta adrenérgica y a neuroglucopenia; el diagnóstico se basa en la hipoglicemia algunas veces provocada por el ayuno, el ejercicio, o el aumento desproporcinado de la insulina circulante en relación con la glicemia, lo que se hace más aparente después del estímulo con tolbutamida o calcio. Se informan cinco casos vistos en nuestra Institución. Otro es el Gastrinoma que secreta gastrina, cursa con hipersecreción gástrica, úlcera péptica de localización atípica, complicada y rebelde al tratamiento, así como diarrea; el diagnóstico se hace por el quimismo gástrico basal y dosificación de la gastrina sérica, tanto en condiciones basales como despúes del estímulo con calcio o secretina, 60% de los gastrinomas son malignos. Se informan siete casos. El Glucagonoma, otro tumor pancreático produce glucagón y se manifiesta por diabetes de fácil control, eritema migratorio necrolítico, desnutrición y anemia hipocrómica; el aumento del glucagón sérico da el diagnóstico. El somatostatinoma se manigfiesta por diabetes, diarrea, esteatorrea y disfunción vesicular con formación de cálculos; el aumento de la somatostatina sérica confirma el diagnóstico. También se han descrito adenomas de células F productoras de polipéptidos pancreáticos, que cursan con diarrea, y Vipomas a partir de las células H, que producen el polipéptido intestinal vasoactivo y se manifiestan por diarrea acuosa, aclorihidria e hipokalemia...

Antral gastrin cell population in patients with chagasic megaesophagus and megacolon

1. Patients with chronic Chagas' disease have abnormally low gastric acid secretion and increased gastrin release both during fasting and after different stimuli. Regardless of the relationship between intragastric acidity and gastrin secretion, it is uncertain whether hypergastrinemia in Chagas' disease is caused by an increased population of antral gastrin (G) cells (hyperplasia) or by enhanced cell activity (hyperfunction). 2. We therefore estimated G cell number in antral biopsies from 16 chagasic patients and 13 control subjects using a peroxidase-anti-peroxidase immunohistochemical technique. All subjects underwent a gastric secretion test to determine peak acid output following intravenous pentagastrin instillation. 3. Antral G cell number in Chagas' disease patients was not significantly different from that observed in the control group (number of cells/mm2, median and (range): 128 (44-284) vs 138 (65-285)). 4. In chagasic patients, peak acid output was significantly lower than in controls (mmol/h, median and (range): 9.819 (3.024-21.564) vs 17.490 (9.423-25.848)). 5. These results suggest that the increase in gastrin release associated with reduced gastric acid secretion in Chagas' disease is mediated by antral G cell hyperfunction rather than by hyperplasia

Epidermal growth factor and gastrin in scleroderma/CREST syndrome

Background. The objective of this study was to determine levels of epidermal growth factor (EGF) and gastrin (GA) in saliva, serum, and urine in scleroderma (Scl) and CREST syndrome. Methods. EGF and GA levels were mesured by radioimmunoassay in saliva, serum and urine in 10 patients (51 years, median; range, 35-66 years); 9 females and 1 male with Scl, 3 females with CREST syndrome, and 18 age-and sex-matched controls, 17 females and 1 male free of any systemic inflammatory disease. Results. In serum, the EGF was lower in Scl/CREST than controls (p=0.02), while GA serum concentrations were higher in Scl/CREST (p=0.02). In urine, EGF in Scl/CREST was slightly lower than controls (p=NS) and GA concentrations were higher than controls (p=0.03). In saliva, the EGF levels in Scl/CREST were also slightly lower than controls (p=NS), while GA concentrations in both Scl/CREST and controls were not different (p=NS). Conclusions. Low concentrations of EGF in serum probably play a role in the pathogenesis of Scl/CREST. GA concentration can be increased as a consequence of the low levels of EGF because of the structural homology of this peptide with urogastrone, a GA inhibitor factor

Hormonas gastrointestinales en la estimulación enteral mínima en neonatos prematuros enfermos / Gastrointestinal hormone and minimal enteral feeding in sick premature infants

Objetivo. Medir la respuesta hormonal con estimulación enteral mínima (EEM) en prematuros enfermos. Metología. Fueron 41 pacientes, con peso al nacimiento <1800 g, distribuidos en: grupo I (temprano) con inicio del estímulo en menos de cinco días de edad (n=26), y grupo II (tardío) entre 10 y 14 días (n=15). Se hicieron mediciones basales de cuatro hormonas gastrointestinales (gastrina, PIG, motilina y neurotensina y se inició la estimulación con fórmula para prematuros diluida, comenzando un un mL cada dos horas e incrementando un mL diario hasta alcanzar aproximadamente 120 mL como volumen total, y se registraron las mediciones de las hormonas. Resultados. No hubo diferencia intergrupos en peso, edad gestacional, trofismo y estancia hospitalaria. Hubo diferencias intragrupos entre las mediciones basal y final en todas las hormonas en ambos grupos. Los resultados por subgrupos de edad gestacional (menores y mayores de 32 semanas) y eutróficos e hipotróficos mostraron diferencial basal-final. En relación con peso al nacer y volumen de leche de la EEM, los resultados fueron variables. No hubo complicaciones con el uso del EEM. Conclusiones. El EEM favorece la secreción hormonal gastrointestinal en prematuros enfermos aun administrado tardíamente. El EEM no incrementó las complicaciones abdominales. El peso, la edad gestacional, y el grado trofismo no se asocian a la magnitud de la secreción hormonal