Impaired Sympathoadrenal Axis Function Contributes to Enhanced Insulin Secretion in Prediabetic Obese Rats

Andreazzi, Ana Eliza; Grassiolli, Sabrina; Marangon, Paula Beatriz; Martins, Adriana Gallego; Oliveira, Júlio Cézar de; Torrezan, Rosana; Gravena, Clarice; García, Raúl; Mathias, Paulo Cézar de Freitas

doi:10.1155/2011/947917

Cited by 20 publications

(16 citation statements)

References 66 publications

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“…Opposed to glycine, neonatal MSG treatment caused shorter NAL and lower Lee Index compared to control animals. This is consistent with other studies showing that MSG treatment induced a growth, endocrine and behavioral deficit [6].…”

Section: Discussionsupporting

confidence: 94%

“…This data corroborates to previous works [6,34]. Glycine administration on the other hand, was able to complete reestablish adrenal catecholamine content and basal secretion in MSG obese rats.…”

Section: Discussionsupporting

confidence: 93%

“…The experimental obesity model induced by monosodium L-glutamate (MSG) has been widely used for being representative of the metabolic disturbance observed in human obesity [6]. The neonatal administration of MSG causes lesion on the arcuate nucleus of hypothalamus [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, the animals develop an abnormal deposition of fat [12][13][14]. Also, MSG-obese animals present hyperinsulinemia, insulin resistance and a notorious accumulation of catecholamines in the adrenal medulla due to impaired secretion process, among other features [6,10,15].…”

Section: Introductionmentioning

confidence: 99%

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Early glycine supplementation re-establishes adrenal catecholamine secretion in hypothalamic obesity model in rats but does not affect visceral adiposity.

Andreazzi

Silva

Chaves

et al. 2015

JGM

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Obesity is a worldwide epidemic that features a multifactorial syndrome characterized by a chronic positive energetic unbalance. Neonatal administration of monosodium L-glutamate (MSG) causes lesion on the arcuate nucleus of hypothalamus that led to development of obesity in the adult life in rodents characterized by a notorious accumulation of catecholamine in the adrenal medulla. The amino acid glycine induces catecholamine secretion of adrenal medulla. Thus, the objective of our work was to evaluate the possible effects of glycine administration in the MSG-obesity model in rats and investigate its impact on adrenal catecholamine medulla homeostasis. Male Wistar rats received MSG solution (4mg/g body weight)subcutaneously in the cervical area for 5 days after delivery, controls received saline solution. Animals were also divided in two groups, in which one received tap water added with glycine (0.1g/Kg) after weaning on 21 st day until 90 days of life. Biometrical variables, visceral fat pads weight, total content and basal secretion of adrenal cathecolamine were evaluated. Glycine increased Lee index of all tested groups and had no effect on visceral adiposity. However, glycine treatment completely reestablished catecholamine total content and basal secretion of MSG-obese group. In conclusion, although glycine treatment apparently completely reestablishes catecholamine secretion homeostasis it is not sufficient to significant directly reduce visceral adiposity in MSG obesity model in rats. DOI : 10.14302/issn.2572-5424.jgm-14-604Corresponding author: Ana Eliza Andreazzi, Laboratory of Physiology, Department of Physiology Federal University of Juiz de Fora, Rua José Lourenço Kelmer, s/n -Campus Universitário , Bairro São Pedro -CEP: 36036-900 -Juiz de Fora -MG/Brazil, E-mail: anaeliza.andreazzi@ufjf.edu.brRunning title: Glycine reestablishes catecholamine secretion in MSG-rats.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Early glycine supplementation re-establishes adrenal catecholamine secretion in hypothalamic obesity model in rats but does not affect visceral adiposity.

Andreazzi

Silva

Chaves

et al. 2015

JGM

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“…Control animals were injected with an equimolar saline solution. The pups were weaned at 21 days of age [16]. …”

Section: Methodsmentioning

confidence: 99%

Protective Effect of Metformin Against Walker 256 Tumor Growth is Not Dependent on Metabolism Improvement

Franco

Miranda

Oliveira

et al. 2014

Cell Physiol Biochem

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Background/Aims: The objective of the current work was to test the effect of metformin on the tumor growth in rats with metabolic syndrome. Methods: We obtained pre-diabetic hyperinsulinemic rats by neonatal treatment with monosodium L-glutamate (MSG), which were chronically treated every day, from weaning to 100 day old, with dose of metformin (250 mg/kg body weight). After the end of metformin treatment, the control and MSG rats, treated or untreated with metformin, were grafted with Walker 256 carcinoma cells. Tumor weight was evaluated 14 days after cancer cell inoculation. The blood insulin, glucose levels and glucose-induced insulin secretion were evaluated. Results: Chronic metformin treatment improved the glycemic homeostasis in pre-diabetic MSG-rats, glucose intolerance, tissue insulin resistance, hyperinsulinemia and decreased the fat tissue accretion. Meanwhile, the metformin treatment did not interfere with the glucose insulinotropic effect on isolated pancreatic islets. Chronic treatment with metformin was able to decrease the Walker 256 tumor weight by 37% in control and MSG rats. The data demonstrated that the anticancer effect of metformin is not related to its role in correcting metabolism imbalances, such as hyperinsulinemia. However, in morphological assay to apoptosis, metformin treatment increased programmed cell death. Conclusion: Metformin may have a direct effect on cancer growth, and it may programs the rat organism to attenuate the growth of Walker 256 carcinoma.

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Perinatal Positive and Negative Influences on the Early Neurobehavioral Reflex and Motor Development

Horváth

Reglődi

Farkas

et al. 2014

Perinatal Programming of Neurodevelopment

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Early life events are critical in the development of the central nervous system. Injuries in this period can cause severe damage with permanent disabilities. The early changes following a perinatal lesion have prognostic significance. The nervous system in young age has a potential for plasticity and regeneration, which can prevent the negative effects of neuronal damage, and the most important objective of rehabilitation is to enhance this inner potential of the developing brain. Experimental examination of the environmental factors affecting this regeneration and remodeling process is very important. Endogenous factors, such as neurotrophic factors, which play a role in neurogenesis, migration, and differentiation of neurons, and development of neuronal circuits, are also in the center of interest. Most studies concerning the effect of positive or negative perinatal treatments focus mainly on long-term effects, and most examinations are carried out on adult animals following perinatal injuries. Less data are available on short-term effects and early neurobehavioral changes. In the past several years, we have shown how different (positive or negative) perinatal events affect the early neuronal development. Applying different tests widely used for behavioral testing, we have established a standardized testing method. This includes measuring parameters of somatic growth and facial development, appearance of basic neurological reflexes and also reflex performance, more complex motor coordination tests, and open-field and novelty-seeking tests. In the present chapter, we summarize data on early neurobehavioral development of newborn rats subjected to negative (perinatal asphyxia, hypoxia, excitotoxic injury, stress) and positive (enriched environment, neurotrophic factor treatment) stimuli during early postnatal life.

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Impaired Sympathoadrenal Axis Function Contributes to Enhanced Insulin Secretion in Prediabetic Obese Rats

Cited by 20 publications

References 66 publications

Early glycine supplementation re-establishes adrenal catecholamine secretion in hypothalamic obesity model in rats but does not affect visceral adiposity.

Early glycine supplementation re-establishes adrenal catecholamine secretion in hypothalamic obesity model in rats but does not affect visceral adiposity.

Protective Effect of Metformin Against Walker 256 Tumor Growth is Not Dependent on Metabolism Improvement

Perinatal Positive and Negative Influences on the Early Neurobehavioral Reflex and Motor Development

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