The influence of vanadate on insulin counter-regulatory hormones in obese fa/fa rats

1991 ◽  
Vol 131 (2) ◽  
pp. 185-191 ◽  
Author(s):  
S. M. Brichard ◽  
L. N. Ongemba ◽  
J. Kolanowski ◽  
J. C. Henquin
Keyword(s):  
Body Weight ◽  
Food Restriction ◽  
Body Weight Gain ◽  
Plasma Corticosterone ◽  
Plasma Glucagon ◽  
Lower Plasma ◽  
Peripheral Tissues ◽  
Insulin Resistant ◽  
Glucose Homoeostasis ◽  
Basal Plasma

ABSTRACT Vanadate has been shown to improve glucose homoeostasis in mildly glucose-intolerant and severely insulin-resistant fa/fa rats. The present study examined whether changes in insulin counter-regulatory hormones contribute to this beneficial effect of vanadate. Since oral administration of Na3VO4 caused a decrease in food intake and stopped the increase in body weight, vanadate-treated fa/fa rats were compared with both controls with food available ad libitum and pair-fed rats. Slightly lower plasma glucose levels were maintained in conjunction with markedly lower plasma insulin levels in vanadatetreated rats, and this effect was not simply due to the smaller body weight of the animals. Compared with control rats, treatment with vanadate affected neither basal plasma glucagon levels nor the increase in glucagon levels observed after insulin-induced hypoglycaemia or after i.v. injection of arginine. Compared with pair-fed rats, treatment with vanadate prevented the fall in basal plasma glucagon and its exaggerated rise in response to insulin that mere food restriction produced. Plasma corticosterone levels were high in fa/fa rats. Vanadate and pair-feeding similarly decreased basal plasma levels of corticosterone as well as nocturnal corticosteronuria. Thus the attenuation of the hypercorticism of fa/fa rats results from the reduction in body weight gain rather than from a specific action of vanadate. Vanadate did not influence urinary excretion of noradrenaline, an index of neural sympathetic activity, but prevented the increase in adrenaline excretion, an index of adrenal medulla activity, that was produced by food restriction in pair-fed rats. In conclusion, vanadate administration has no or little specific effects on three major insulin counter-regulatory hormones. This reinforces the suggestion that the beneficial effects of vanadate on glucose homoeostasis in fa/fa rats are mainly due to a correction of insulin resistance in peripheral tissues. Journal of Endocrinology (1991) 131, 185–191

scholarly journals Maternal undernutrition during late gestation-induced intrauterine growth restriction in the rat is associated with impaired placental GLUT3 expression, but does not correlate with endogenous corticosterone levels

2002 ◽  
Vol 174 (1) ◽  
pp. 37-43 ◽  
Author(s):  
J Lesage ◽  
D Hahn ◽  
M Leonhardt ◽  
B Blondeau ◽  
B Breant ◽  
...  
Keyword(s):  
Body Weight ◽  
Plasma Glucose ◽  
Food Restriction ◽  
Glucose Transporter ◽  
Maternal Plasma ◽  
Plasma Corticosterone ◽  
Growth Restriction ◽  
Late Gestation ◽  
Glucose Content ◽  
Protein Levels

Fetal intrauterine growth restriction (IUGR) is a frequently occurring and serious complication of pregnancy. Infants exposed to IUGR are at risk for numerous perinatal morbidities, including hypoglycemia in the neonatal period, as well as increased risk of later physical and/or mental impairments, cardiovascular disease and non-insulin-dependent diabetes mellitus. Fetal growth restriction most often results from uteroplacental dysfunction during the later stage of pregnancy. As glucose, which is the most abundant nutrient crossing the placenta, fulfills a large portion of the fetal energy requirements during gestational development, and since impaired placental glucose transport is thought to result in growth restriction, we investigated the effects of maternal 50% food restriction (FR50) during the last week of gestation on rat placental expression of glucose transporters, GLUT1, GLUT3 and GLUT4, and on plasma glucose content in both maternal and fetal compartments. Moreover, as maternal FR50 induces fetal overexposure to glucocorticoids and since these hormones are potent regulators of placental glucose transporter expression, we investigated whether putative alterations in placental GLUT expression correlate with changes in maternal and/or fetal corticosterone levels. At term (day 21 of pregnancy), plasma glucose content was significantly reduced (P<0.05) in mothers subjected to FR50, but was not affected in fetuses. Food restriction reduced maternal body weight (P<0.001) but did not affect placental weight. Plasma corticosterone concentration, at term, was increased (P<0.05) in FR50 mothers. Fetuses from FR50 mothers showed reduced body weight (P<0.001) but higher plasma corticosterone levels (P<0.05). Adrenalectomy (ADX) followed by corticosterone supplementation of the mother prevented the FR50-induced rise in maternal plasma corticosterone at term. Food restriction performed on either sham-ADX or ADX mothers induced a similar reduction in the body weight of the pups at term (P<0.01). Moreover, plasma corticosterone levels were increased in pups from sham-ADX FR50 mothers (P<0.01) and in pups from ADX control mothers (P<0.01). Western blot analysis of placental GLUT proteins showed that maternal FR50 decreased placental GLUT3 protein levels in all experimental groups at term (P<0.05 and P<0.01), but did not affect either GLUT1 or GLUT4 protein levels. Northern blot analysis of placental GLUT expression showed that both GLUT1 and GLUT3 mRNA were not affected by the maternal feeding regimen or surgery. We concluded that prolonged maternal malnutrition during late gestation decreases maternal plasma glucose content and placental GLUT3 glucose transporter expression, but does not obviously affect fetal plasma glucose concentration. Moreover, the present results are not compatible with a role of maternal corticosterone in the development of growth-restricted rat fetuses.

scholarly journals Nociceptive Sensory Neurons Mediate Inflammation Induced by Bacillus Anthracis Edema Toxin

2021 ◽  
Vol 12 ◽  
Author(s):  
Nicole J. Yang ◽  
Dylan V. Neel ◽  
Liwen Deng ◽  
Michelle Heyang ◽  
Angela Kennedy-Curran ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Bacillus Anthracis ◽  
Body Weight Gain ◽  
Subcutaneous Administration ◽  
Active Role ◽  
Cellular Mechanisms ◽  
Peripheral Tissues ◽  
Nociceptive Neurons ◽  
Edema Toxin

Bacterial products are able to act on nociceptive neurons during pathogenic infection. Neurogenic inflammation is an active part of pain signaling and has recently been shown to impact host-pathogen defense. Bacillus anthracis Edema Toxin (ET) produces striking edema in peripheral tissues, but the cellular mechanisms involved in tissue swelling are not completely understood. Here, we find that nociceptive neurons play a role in ET-induced edema and inflammation in mice. Subcutaneous footpad infection of B. anthracis Sterne caused ET-dependent local mechanical allodynia, paw swelling and body weight gain. Subcutaneous administration of ET induced paw swelling and vascular leakage, the early phases of which were attenuated in the absence of Trpv1+ or Nav1.8+ nociceptive neurons. Nociceptive neurons express the anthrax toxin receptor ANTXR2, but this did not mediate ET-induced edema. ET induced local cytokine expression and neutrophil recruitment, which were dependent in part on Trpv1+ nociceptive neurons. Ablation of Trpv1+ or Nav1.8+ nociceptive neurons also attenuated early increases in paw swelling and body weight gain during live B. anthracis infection. Our findings indicate that nociceptive neurons play an active role in inflammation caused by B. anthracis and Edema Toxin to potentially influence bacterial pathogenesis.

scholarly journals INTOXICAÇÃO SUBAGUDA AO MANGANÊS EM RATOS WISTAR ADULTOS: AVALIAÇÃO DE PARÂMETROS OXIDATIVOS NO SNC E DEPOSIÇÃO DO METAL EM DIFERENTES TECIDOS

2018 ◽  
Vol 7 (2) ◽  
pp. 193-210
Author(s):  
Maria Victória Branco Flores ◽  
Tuany Eichwald ◽  
Analú Mantovani ◽  
Viviane Glaser ◽  
Carine Raquel Richter Schimitz ◽  
...  
Keyword(s):  
Body Weight ◽  
Mitochondrial Function ◽  
Complex I ◽  
Body Weight Gain ◽  
Thiobarbituric Acid ◽  
Significant Inhibition ◽  
The Body ◽  
Control Group ◽  
Peripheral Tissues ◽  
The Brain

O Manganês (Mn) é um metal essencial para o organismo. É distribuído no ambiente e utilizado em processos industriais. Apesar de essencial, é neurotóxico à exposições cumulativas, causando uma desordem neurológica, o Manganismo. O estudo avaliou o efeito da administração subaguda de Mn sob a forma de cloreto e acetato de Mn, sobre a função mitocondrial e parâmetros oxidativos no encéfalo, bem como o acúmulo deste metal no encéfalo e tecidos periféricos de ratos adultos. Os ratos receberam 6 mg/kg de Mn i.p. na forma de cloreto ou acetato de Mn, 5 dias/semana por 4 semanas. O grupo controle recebeu solução salina 0,9% pela mesma via de administração e mesmo período. Foi mensurada a concentração de substâncias reativas ao ácido tiobarbitúrico (TBARS) e grupamentos NPSH, a atividade dos complexos I e II da cadeia respiratória no encéfalo e/ou estruturas cerebrais, bem como o peso corporal e a concentração de Mn e Fe no soro, encéfalo, tecido renal e hepático. Foi observada uma diminuição no ganho de peso corporal dos animais que receberam o Mn, um aumento na concentração/depósito de Mn no soro, encéfalo e tecido renal, tanto na forma de cloreto e acetato de Mn, quando comparados com o grupo controle. Além disso, houve um aumento significativo no conteúdo de NPSH no encéfalo e, embora não significativo, uma tendência de aumento da concentração de TBARS, no grupo que recebeu cloreto de Mn. Ainda, foi verificada uma inibição na atividade do complexo I no estriado dos animais expostos ao cloreto de Mn. Não houve diferença entre os grupos nas atividades do complexo I e II no encéfalo e hipocampo. Em conjunto, os dados indicam que a exposição ao Mn em baixas doses contribui para o desenvolvimento de estresse oxidativo e disfunção mitocondrial no SNC, com aparente predileção de dano ao estriado.Palavras-chave: Manganês. Exposição subaguda. Parâmetros oxidativos. Função mitocondrial. MANGANESE SUBACUTE INTOXICATION IN ADULT WISTAR RATS: EVALUATION OF OXIDATIVE PARAMETERS IN CNS AND METAL DEPOSITION IN DIFFERENT TISSUES ABSTRACT: Mn is an essential metal to the organism. It is distributed in the environment and used in industrial processes. Although essential, it is neurotoxic to cumulative exposures, and can cause a neurological disorder, called Manganism. This study evaluated the effect of subacute Mn as chloride and acetate of Mn administration on mitochondrial function and oxidative parameters in adult rat brain, as well as the accumulation of this metal in the brain and peripheral tissues. The rats received 6 mg/kg of Mn i.p., as Mn chloride or Mn acetate, 5 days/week for 4 weeks. The control group received 0.9% of saline solution in the same way of administration and in the same period. It was measured the concentration of thiobarbituric acid reactive substances (TBARS) and NPSH groups, the activity of mitochondrial complex I and II in brain and/or in the brain structures, as well as the body weight and the concentration of Mn and Fe accumulation. It was observed a decrease on body weight gain in animals exposed to Mn and an increase of concentration/deposit of Mn in serum, brain and kidney, in the both Mn chloride and acetate form when compared to the control group. In addition, there was a significant increase in brain NPSH content and, although it was not significant, a trend of increasing on TBARS concentration in the group that received Mn. Besides that, a significant inhibition of complex I activity was observed in the striatum of the animals exposed to Mn. There was not difference between groups on complex I and II in the brain and hippocampus. Together, these data indicate that exposure to Mn at low doses contributes to the development of oxidative stress and mitochondrial dysfunction in the CNS, with apparent predilection of striatum damage.Keywords: Manganese. Subacute exposure. Oxidative parameters. Mitochondrial function.

scholarly journals Choline Deficiency Attenuates Body Weight Gain and Improves Glucose Tolerance in ob/ob Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Gengshu Wu ◽  
Liyan Zhang ◽  
Tete Li ◽  
Gary Lopaschuk ◽  
Dennis E. Vance ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Weight Gain ◽  
Fat Mass ◽  
Body Weight Gain ◽  
Genetic Defect ◽  
Plasma Glucagon ◽  
Choline Deficiency ◽  
Deficient Diet ◽  
Insulin Tolerance

Previous studies demonstrated that choline supply is directly linked to high-fat-diet-induced obesity and insulin resistance in mice. The aim of this study was to evaluate if choline supply could also modulate obesity and insulin resistance caused by a genetic defect. Eight-week-old male ob/ob mice were fed for two months with either choline-deficient or choline-supplemented diet. Tissue weight including fat mass and lean mass was assessed. Intracellular signaling, plasma glucagon and insulin, and glucose and insulin tolerance tests were also investigated. The choline-deficient diet slowed body weight gain and decreased fat mass. Choline deficiency also decreased plasma glucose level and improved glucose and insulin tolerance although fatty liver was exacerbated. Increased adipose lipolytic activity, decreased plasma glucagon and reduced expression of hepatic glucagon receptor were also observed with the choline-deficient diet. Our results demonstrate that a choline-deficient diet can decrease fat mass and improve glucose tolerance in obese and diabetic mice caused by a genetic defect.

Skeletal muscle glucose metabolism in obesity-prone and obesity-resistant rats

1993 ◽  
Vol 264 (6) ◽  
pp. R1224-R1228 ◽  
Author(s):  
M. J. Pagliassotti ◽  
K. A. Shahrokhi ◽  
J. O. Hill
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Weight Gain ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Glycogen Synthase ◽  
Body Weight Gain ◽  
Glycogen Synthesis ◽  
Insulin Resistant ◽  
Wide Range

Ad libitum access to a high-fat (HF) diet produces a wide range of weight gain in rats. Rats most susceptible to weight gain on such a diet (obesity prone; OP) are more insulin resistant after 4-5 wk of diet exposure than are those most resistant (obesity resistant; OR) to weight gain. To investigate whether skeletal muscle glucose metabolism contributes to insulin resistance in this model, insulin-stimulated glucose metabolism was assessed in the perfused hindquarter of rats exposed to either a low-fat (LF, n = 6) or HF diet for 5 wk. Delineation of OP (n = 6) and OR (n = 6) rats was based on body weight gain. OP rats gained 60% more body weight while eating only 10% more energy than OR rats. Single-pass perfusions were carried out for 2 h in the presence of glucose, insulin, and [U-14C]glucose. Insulin-stimulated glucose uptake (mumol.100 g-1.min-1) was 14.2 +/- 0.9 in LF, 11.1 +/- 0.8 in OR, and 6.2 +/- 0.6 in OP. Glucose oxidation (mumol.100 g-1.min-1) was 1.7 +/- 0.3 and 1.2 +/- 0.3 in LF and OR, respectively, but was 0.2 +/- 0.1 in OP. Net glycogen synthesis was significantly reduced in OP compared with OR and LF despite similar glycogen synthase I activity. Muscle triglyceride concentration was not significantly different in OR and OP rats. These results demonstrate significant defects in skeletal muscle glucose uptake and disposal in rats most susceptible to HF diet-induced obesity. Clearly, the heterogeneous response to a HF diet involves not only body weight gain but also skeletal muscle fuel metabolism.

scholarly journals SIRT1 in Astrocytes Regulates Glucose Metabolism and Reproductive Function

Endocrinology ◽  
2019 ◽  
Vol 160 (6) ◽  
pp. 1547-1560 ◽  
Author(s):  
Irene Choi ◽  
Emily Rickert ◽  
Marina Fernandez ◽  
Nicholas J G Webster
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Body Weight Gain ◽  
Reproductive Function ◽  
Sirtuin 1 ◽  
Corpora Lutea ◽  
Class Iii ◽  
Peripheral Tissues ◽  
Reproductive Regulation ◽  
Insulin Tolerance

Abstract Sirtuin 1 (Sirt1) is an NAD-dependent class III deacetylase that functions as a cellular energy sensor. In addition to its well-characterized effects in peripheral tissues, evidence suggests that SIRT1 in neurons plays a role in the central regulation of energy balance and reproduction, but no studies have addressed the contribution of astrocytes. We show here that overexpression of SIRT1 in astrocytes causes markedly increased food intake, body weight gain, and glucose intolerance, but expression of a deacetylase-deficient SIRT1 mutant decreases food intake and body weight and improves glucose tolerance, particularly in female mice. Paradoxically, the effect of these SIRT1 mutants on insulin tolerance was reversed, with overexpression showing greater insulin sensitivity. The mice overexpressing SIRT1 were more active, generated more heat, and had elevated oxygen consumption, possibly in compensation for the increased food intake. The female overexpressing mice were also more sensitive to diet-induced obesity. Reproductively, the mice expressing the deacetylase-deficient SIRT1 mutant had impaired estrous cycles, decreased LH surges, and fewer corpora lutea, indicating decreased ovulation. The GnRH neurons were responsive to kisspeptin stimulation, but hypothalamic expression of Kiss1 was reduced in the mutant mice. Our results showed that SIRT1 signaling in astrocytes can contribute to metabolic and reproductive regulation independent of SIRT1 effects in neurons.

Effects of the uterus and the ovaries on growth, somatotrophin and somatomedin A in developing rats

1987 ◽  
Vol 113 (1) ◽  
pp. 21-26
Author(s):  
J. C. Biro ◽  
P. Eneroth
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Plasma Concentrations ◽  
Lower Plasma ◽  
Final Body Weight ◽  
Old Rats ◽  
Plasma Hormone

ABSTRACT The effects of hysterectomy and ovariectomy on plasma concentrations of GH, somatomedin A, TSH and thyroxine (T4) were studied in developing rats. Four groups of 24-day-old rats were ovariectomized, ovohysterectomized, hysterectomized or sham-operated. Their weights, lengths and plasma hormone concentrations were measured at 26, 43, 64, 78 and 92 days of age to investigate pre- and postpubertal differences caused by the uterus or ovaries. Plasma concentrations of the hormones examined showed a successive rise with time, but GH and somatomedin A concentrations rose mainly after the opening of the vagina (days 50–55). Higher GH and somatomedin A concentrations were found in the plasma of ovariectomized animals than in ovohysterectomized controls before puberty (GH: 260–300%, P<0·01; somatomedin A: 25–30%, P<0·05). Ovariectomized animals weighed more than ovohysterectomized females after puberty (4·5–6%, P<0·01). This indicated that the uterus exerted a stimulatory effect on GH-somatomedin A regulation and body weight gain in the absence of the ovaries. Significantly lower plasma somatomedin A (but not GH) concentrations were found in hysterectomized and sham-operated animals than in their respective controls after puberty (30–39%, P<0·01) and their final body weight was lower (22–26%, P<0·001). There were no consecutive uterus- or ovary-related changes in plasma TSH and T4 levels. It was concluded that both the uterus and ovaries had significant as well as opposite effects on somatomedin A and body weight with the effects of the ovaries being greater than those of the uterus. J. Endocr. (1987) 113, 21–26

Influence of Initial Food Restriction on Subsequent Body Weight Gain and Body Fat Accumulation in Rats

1978 ◽  
Vol 108 (11) ◽  
pp. 1724-1732 ◽  
Author(s):  
Aysel Ozelci ◽  
Dale R. Romsos ◽  
Gilbert A. Leveille
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Fat ◽  
Food Restriction ◽  
Body Weight Gain ◽  
Fat Accumulation
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