Gut hormones of preterm infants with abdominal symptoms and hypothyroxinemia
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The pathogenesis of abdominal symptoms in premature infants with hypothyroxinemia is not understood; therefore, we investigated changes in gut hormones before and after levothyroxine sodium (T4-Na) supplementation in preterm infants with abdominal symptoms and hypothyroxinemia.In eight preterm study subjects and 14 gestational age-matched controls, fasting serum concentration of leptin, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), peptide YY (PYY), pancreatic polypeptide, insulin, amylin and ghrelin was measured using a bead array system.Serum GLP-1, GIP and PYY in the subjects before T4-Na supplementation were lower than in controls at age 2 weeks. After improvement of abdominal symptoms and free thyroxine, serum levels of the three gut hormones in the subjects were increased and were not different from those in the control patients.In preterm infants with abdominal symptoms, serum GLP-1, GIP and PYY might be related to thyroid function.Keywords:
Peptide YY
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Obesity is a growing epidemic, causally associated with a number of serious medical conditions, including diabetes mellitus, coronary heart disease, and several cancers. The gut hormones ghrelin and peptide YY are secreted from the gut in response to changes to nutritional status. While food intake is stimulated by ghrelin, it is inhibited by peptide YY. The discovery, anatomy, and physiology of ghrelin and peptide YY are discussed, focusing on the adaptive changes in diseases such as obesity and anorexia nervosa. Ghrelin and PYY are important therapeutic targets in the quest to find an effective antiobesity treatment.
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Fourteen cases of gastrointestinal endocrine tumors were examined im‐munohistochemically for peptide YY, pancreatic polypeptide, glucagon, and somatostatin. Peptide YY cells were present in seven tumors, pancreatic polypeptide cells in eight tumors, glucagon cells in six tumors, and somatostatin cells in nine tumors. All 7 rectal endocrine tumors examined were found to contain peptide YY, while in the tumors of the other sites peptide YY cells were not detected. Peptide YY cell population in the rectal tumors was small to moderate in comparison with pancreatic polypeptide and glucagon cell population. This study suggests that peptide YY cells may be a common constituent of rectal endocrine tumors together with pancreatic polypeptide and glucagon cells, and that the peptide YY spectrum of gastrointestinal endocrine tumors may be closely related to the location of the tumors. Moreover, it can also be said that peptide YY may be used as one of the markers of rectal endocrine tumors.
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Based on structural and evolutionary criteria, neuropeptide Y (NPY)b, peptide YY (PYY) and pancreatic polypetide (PP) are closely related polypeptides ([Larhammar, 1996a][1]). They are composed of 36 amino acids each and share considerable amino acid homology, amidated C-terminal ends, and the
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Circulating levels of the pancreatic β-cell peptide hormone amylin and the gut peptide PYY[3–36] increase after nutrient ingestion. Both have been implicated as short-term signals of meal termination with anorexigenic and weight-reducing effects. However, their combined effects are unknown. We report that the combination of amylin and PYY[3–36] elicited greater anorexigenic and weight-reducing effects than either peptide alone. In high-fat-fed rats, a single ip injection of amylin (10 μg/kg) plus PYY[3–36] (1000 μg/kg) reduced food intake for 24 h (P < 0.05 vs. vehicle), whereas the anorexigenic effects of either PYY[3–36] or amylin alone began to diminish 6 h after injection. These anorexigenic effects were dissociable from changes in locomotor activity. Subcutaneous infusion of amylin plus PYY[3–36] for 14 d suppressed food intake and body weight to a greater extent than either agent alone in both rat and mouse diet-induced obesity (DIO) models (P < 0.05). In DIO-prone rats, 24-h metabolic rate was maintained despite weight loss, and amylin plus PYY[3–36] (but not monotherapy) increased 24-h fat oxidation (P < 0.05 vs. vehicle). Finally, a 4 × 3 factorial design was used to formally describe the interaction between amylin and PYY[3–36]. DIO-prone rats were treated with amylin (0, 4, 20, and 100 μg/kg·d) and PYY[3–36] (0, 200, 400 μg/kg·d) alone and in combination for 14 d. Statistical analyses revealed that food intake suppression with amylin plus PYY[3–36] treatment was synergistic, whereas body weight reduction was additive. Collectively, these observations highlight the importance of studying peptide hormones in combination and suggest that integrated neurohormonal approaches may hold promise as treatments for obesity.
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Article Plasma Peptide YY and Ghrelin Levels in Infants and Children with Prader-Willi Syndrome was published on September 1, 2004 in the journal Journal of Pediatric Endocrinology and Metabolism (volume 17, issue 9).
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Peptide YY
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Enteroendocrine cell
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Peptide YY
Pancreatic polypeptide
Enteroendocrine cell
Gastrointestinal hormone
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Ghrelin and peptide YY (PYY) are brain-gut peptides that have a variety of physiological functions and are involved in energy regulation. Thus far, abnormalities in the expression and secretion of ghrelin and PYY are known to occur in lifestyle-related diseases, including obesity, and the improvement of these abnormalities has become an important challenge. Exercise has recently been reported to influence ghrelin and PYY concentrations. Exercise increases the PYY secretion. The effects of exercise on ghrelin levels vary with the study subject, timing of exercise, and duration of exercise. Here, we review the findings of recent studies on the association of PYY and ghrelin with obesity, particularly, on the influence of exercise on PYY and ghrelin levels.
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