Adrenal medullary function and expression of catecholamine-synthesizing enzymes in mice with hypothalamic obesity

Martins, Andréia C.P.; Souza, Kleber L.A.; Shio, Marina Tiemi; Mathias, Paulo Cézar de Freitas; Lelkes, Peter I.; García, Raúl

doi:10.1016/j.lfs.2003.10.034

Cited by 38 publications

(24 citation statements)

References 59 publications

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“…In addition, insulin hypersecretion observed in islets from MSG-treated rats can be an adaptation to surpass insulin resistance. However, the maintenance of this insulin hypersecretion over time deteriorates the functional secretory capacity of β-cells and accelerates overt T2D installation [35]. It has been established that physical training restores insulin sensitivity; however, the impact of physical training on the control of insulin secretion from β-cells remains poorly understood.…”

Section: Discussionmentioning

confidence: 99%

Glycolytic and Mitochondrial Metabolism in Pancreatic Islets from MSG-Treated Obese Rats Subjected to Swimming Training

Leite

Ferreira

Rickli

et al. 2013

Cell Physiol Biochem

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Backgrounds/Aims: Obese rats obtained by neonatal monosodium glutamate (MSG) administration present insulin hypersecretion. The metabolic mechanism by which glucose catabolism is coupled to insulin secretion in the pancreatic β-cells from MSG-treated rats is understood. The purpose of this study was to evaluate glucose metabolism in pancreatic islets from MSG-treated rats subjected to swimming training. Methods: MSG-treated and control (CON) rats swam for 30 minutes (3 times/week) over a period of 10 weeks. Pancreatic islets were isolated and incubated with glucose in the presence of glycolytic or mitochondrial inhibitors. Results: Swimming training attenuated fat pad accumulation, avoiding changes in the plasma levels of lipids, glucose and insulin in MSG-treated rats. Adipocyte and islet hypertrophy observed in MSG-treated rats were attenuated by exercise. Pancreatic islets from MSG-treated obese rats also showed insulin hypersecretion, greater glucose transporter 2 (GLUT2) expression, increased glycolytic flux and reduced mitochondrial complex III activity. Conclusion: Swimming training attenuated islet hypertrophy and normalised GLUT2 expression, contributing to a reduction in the glucose responsiveness of pancreatic islets from MSG-treated rats without altering glycolytic flux. However, physical training increased the activity of mitochondrial complex III in pancreatic islets from MSG-treated rats without a subsequent increase in glucose-induced insulin secretion.

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Section: Discussionmentioning

confidence: 99%

Glycolytic and Mitochondrial Metabolism in Pancreatic Islets from MSG-Treated Obese Rats Subjected to Swimming Training

Leite

Ferreira

Rickli

et al. 2013

Cell Physiol Biochem

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“…There have been several experiments producing evidence that MSG rodents present low sympathetic activity (Yoshida et al 1990, Bray 1991, Scomparin et al 2006. Studies in our laboratory have shown reduced secretory capacity of adrenal medullar chromaffin cells from MSG mice, coupled to low catecholamine stores and reduced expression of tirosine hydroxylase (TH), a limiting enzyme to catecholamine biosynthesis (Martins et al 2001(Martins et al , 2004. Whereas acute and long term exercises stimulate sympathetic driving, blood levels of catecholamine and its turnover are increased by exercise (Stallknecht et al 1996).…”

Section: Discussionmentioning

confidence: 99%

Swimming exercise at weaning improves glycemic control and inhibits the onset of monosodium l-glutamate-obesity in mice

Andreazzi¹,

Scomparin²,

Mesquita³

et al. 2009

Journal of Endocrinology

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Swimming exercises by weaning pups inhibited hypothalamic obesity onset and recovered sympathoadrenal axis activity, but this was not observed when exercise training was applied to young adult mice. However, the mechanisms producing this improved metabolism are still not fully understood. Low-intensity swimming training started at an early age and was undertaken to observe glycemic control in hypothalamic-obese mice produced by neonatal treatment with monosodium L-glutamate (MSG). Whereas MSG and control mice swam for 15 min/day, 3 days a week, from the weaning stage up to 90 days old, sedentary MSG and normal mice did not exercise at all. After 14 h of fasting, animals were killed at 90 days of age. Perigonadal fat accumulation was measured to estimate obesity. Fasting blood glucose and insulin concentrations were also measured. Fresh isolated pancreatic islets were used to test glucose-induced insulin release and total catecholamine from the adrenal glands was measured. Mice were also submitted to intraperitoneal glucose tolerance test. MSG-obese mice showed fasting hyperglycemia, hyperinsulinemia, and glucose intolerance. Severe reduction of adrenal catecholamines content has also been reported. Besides, the inhibition of fat tissue accretion, exercise caused normalization of insulin blood levels and glycemic control. The pancreatic islets of obese mice, with impaired glucose-induced insulin secretion, were recovered after swimming exercises. Adrenal catecholamine content was increased by swimming. Results show that attenuation of MSG-hypothalamic obesity onset is caused, at least in part, by modulation of sympathoadrenal axis activity imposed by early exercise, which may be associated with subsequent glucose metabolism improvement.

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“…In a single dose during the neonatal period, although it did not develop obesity, MSG caused a drop in the hypothalamic dopamine 10 . The involvement of enzyme activity of the small bowel in the induction of obesity after the use of MSG and the influence of the adrenal gland have been researched [11][12][13] . MSG has shown a number of changes related to the lack of control of the hypothalamo-pituitary axis with a dosedependent curve including hypophagia, obesity, hypoactivity, reduction of ovarian weight, late puberty and high serum levels of corticosteroids 14,15 .…”

Section: Monosodium Glutamate (Msg)mentioning

confidence: 99%

Experimental model to induce obesity in rats

Diemen

Trindade

2006

Acta Cir. Bras.

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The etiology of obesity is multifactorial and is becoming a problem of public health, due to its increased prevalence and the consequent repercussion of its comorbidities on the health of the population. The great similarity and homology between the genomes of rodents and humans make these animal models a major tool to study conditions affecting humans, which can be simulated in rats. Obesity can be induced in animals by neuroendocrine, dietary or genetic changes. The most widely used models to induce obesity in rats are a lesion of the ventromedial hypothalamic nucleus (VMH) by administering monosodium glutamate or a direct electrical lesion, ovariectomy, feeding on hypercaloric diets and genetic manipulation for obesity. Key words: Obesity. Models, Animal. Metabolism. Rats. RESUMOA obesidade tem etiologia multifatorial e está se tornando um problema de saúde pública devido ao aumento da sua prevalência e a conseqüente repercusão das suas comorbidades na saúde da população. A grande similaridade e homologia entre os genomas dos roedores e dos humanos tornam esses modelos animais uma importante ferramenta para o estudo de condições que afetam os humanos e que podem ser simuladas em ratos. A obesidade pode ser induzida em animais com alterações neuroendócrinas, dietéticas ou genéticas. Os modelos mais utilizados para indução de obesidade em ratos são lesão do núcleo hipotalâmico venteromedial (VMH) através da administração de glutamato monossódico ou lesão elétrica direta, ooforectomia, alimentação com dietas hipercalóricas e manipulação genética para obesidade. Descritores: Obesidade. Modelos Animais. Metabolismo. Ratos.

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Adrenal medullary function and expression of catecholamine-synthesizing enzymes in mice with hypothalamic obesity

Cited by 38 publications

References 59 publications

Glycolytic and Mitochondrial Metabolism in Pancreatic Islets from MSG-Treated Obese Rats Subjected to Swimming Training

Glycolytic and Mitochondrial Metabolism in Pancreatic Islets from MSG-Treated Obese Rats Subjected to Swimming Training

Swimming exercise at weaning improves glycemic control and inhibits the onset of monosodium l-glutamate-obesity in mice

Experimental model to induce obesity in rats

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