about
Acephate exposure during a perinatal life program to type 2 diabetes.Protein Restriction During the Last Third of Pregnancy Malprograms the Neuroendocrine Axes to Induce Metabolic Syndrome in Adult Male Rat OffspringLow-intensity and moderate exercise training improves autonomic nervous system activity imbalanced by postnatal early overfeeding in rats.Maternal protein malnutrition does not impair insulin secretion from pancreatic islets of offspring after transplantation into diabetic rats.Acute exposure to a precursor of advanced glycation end products induces a dual effect on the rat pancreatic islet function.Early treatment with metformin induces resistance against tumor growth in adult rats.CK2 acts as a potent negative regulator of receptor-mediated insulin release in vitro and in vivo.Maternal Diet Supplementation with n-6/n-3 Essential Fatty Acids in a 1.2 : 1.0 Ratio Attenuates Metabolic Dysfunction in MSG-Induced Obese Mice.Pancreatic islets and their roles in metabolic programming.Maternal diet, bioactive molecules, and exercising as reprogramming tools of metabolic programming.Chronic Glibenclamide Treatment Attenuates Walker-256 Tumour Growth in Prediabetic Obese Rats.Glibenclamide treatment blocks metabolic dysfunctions and improves vagal activity in monosodium glutamate-obese male rats.Protein-energy malnutrition at mid-adulthood does not imprint long-term metabolic consequences in male rats.Short-term moderate exercise provides long-lasting protective effects against metabolic dysfunction in rats fed a high-fat diet.Protective effect of metformin against walker 256 tumor growth is not dependent on metabolism improvement.Anesthetic-induced transient hyperglycemia and insulin resistance do not depend on the sympathoadrenal axis.An increase in glucose concentration in the lateral ventricles of the brain induces changes in autonomic nervous system activity.Poor pubertal protein nutrition disturbs glucose-induced insulin secretion process in pancreatic islets and programs rats in adulthood to increase fat accumulation.Short- and long-term effects of maternal perinatal undernutrition are lowered by cross-fostering during lactation in the male rat.Impaired β-cell function in the adult offspring of rats fed a protein-restricted diet during lactation is associated with changes in muscarinic acetylcholine receptor subtypes.Moderate exercise restores pancreatic beta-cell function and autonomic nervous system activity in obese rats induced by high-fat diet.Swim training of monosodium L-glutamate-obese mice improves the impaired insulin receptor tyrosine phosphorylation in pancreatic islets.Sympathetic innervation is essential for metabolic homeostasis and pancreatic beta cell function in adult rats.Methylglyoxal treatment in lactating mothers leads to type 2 diabetes phenotype in male rat offspring at adulthood.HPA axis and vagus nervous function are involved in impaired insulin secretion of MSG-obese rats.Low-protein diet in adult male rats has long-term effects on metabolism.Cross-fostering reduces obesity induced by early exposure to monosodium glutamate in male rats.Impaired muscarinic type 3 (M3) receptor/PKC and PKA pathways in islets from MSG-obese rats.Vagus nerve contributes to metabolic syndrome in high-fat diet-fed young and adult rats.Low-protein diet in puberty impairs testosterone output and energy metabolism in male rats.Intra-islet glucagon signaling is critical for maintaining glucose homeostasis.Early exposure to a high-fat diet has more drastic consequences on metabolism compared with exposure during adulthood in ratsInsulin oversecretion in MSG-obese rats is related to alterations in cholinergic muscarinic receptor subtypes in pancreatic isletsCholinergic-pathway-weakness-associated pancreatic islet dysfunction: a low-protein-diet imprint effect on weaned rat offspringβ-Cell-intrinsic β-arrestin 1 signaling enhances sulfonylurea-induced insulin secretionNovel metabolic role for BDNF in pancreatic β-cell insulin secretionBeneficial metabolic role of β-arrestin-1 expressed by AgRP neuronsAdipocyte Gi signaling is essential for maintaining whole-body glucose homeostasis and insulin sensitivityβ-arrestin-1 suppresses myogenic reprogramming of brown fat to maintain euglycemia
P50
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P50
description
hulumtues
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researcher
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wetenschapper
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հետազոտող
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name
Luiz Felipe Barella
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Luiz Felipe Barella
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Luiz Felipe Barella
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Luiz Felipe Barella
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Luiz Felipe Barella
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type
label
Luiz Felipe Barella
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Luiz Felipe Barella
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Luiz Felipe Barella
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Luiz Felipe Barella
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Luiz Felipe Barella
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Luiz Felipe Barella
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Luiz Felipe Barella
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Luiz Felipe Barella
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Luiz Felipe Barella
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Luiz Felipe Barella
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P1053
C-1181-2014
P106
P1153
55033586000
P2038
Luiz_Felipe_Barella
P21
P31
P3829
P496
0000-0003-2211-3842