Adrenal involvement in the biostimulatory effect of bulls

Background  

The objective was to evaluate if cortisol concentrations are associated with the resumption of luteal activity in postpartum, primiparous cows exposed to bulls. The hypotheses were that 1) interval from start of exposure to resumption of luteal activity; 2) proportions of cows that resumed luteal function during the exposure period; and 3) cortisol concentrations do not differ among cows exposed or not exposed to bulls (Exp. 1), and cows continuously exposed to bull or steer urine (Exp. 2).     

The involvement of purinergic signalling in obesity

Obesity is a growing worldwide health problem, with an alarming increasing prevalence in developed countries, caused by a dysregulation of energy balance. Currently, no wholly successful pharmacological treatments are available for obesity and related adverse consequences. In recent years, hints obtained from several experimental animal models support the notion that purinergic signalling, acting through ATP-gated ion channels (P2X), G protein-coupled receptors (P2Y) and adenosine receptors (P1), is involved in obesity, both at peripheral and central levels. This review has drawn together, for the first time, the evidence for a promising, much needed novel therapeutic purinergic signalling approach for the treatment of obesity with a ‘proof of concept’ that hopefully could lead to further investigations and clinical trials for the management of obesity.     

Adrenal gland involvement in the regulation of renal 11beta-hydroxysteroid dehydrogenase 2

Renal 11beta-hydroxysteroid dehydrogenase 2 (HSD2) catalyzes the conversion of active glucocorticoids to inert 11beta-keto compounds, thereby preventing the illicit binding of these hormones to mineralocorticoid receptors (MRs) and, thus, conferring aldosterone specificity. Absence or inhibition of HSD2 activity, originates a hypertensive syndrome with sodium retention and increased potassium elimination. Recent studies from our laboratory reported an increment of HSD2 activity in intact-stressed rats. To evaluate the adrenal involvement in this increase, we analyzed HSD2 activity and protein abundance in Intact, Sham-operated, and adrenalectomized rats under stress situations (gavage with an overload of 200 mM HCl (10 ml) and simulated gavage) or with corticosterone replacement. HSD2 activity was assessed in renal microsomal preparations obtained from different groups of animals. HSD2 protein abundance was measured by Western-blot. Circulating corticosterone was determined by radioimmunoassay. Sham-operated animals showed an increase in HSD2 activity and abundance compared to Intact and adrenalectomized rats suggesting the involvement of stress-related adrenal factors in HSD2 regulation. In the case of acidotic adrenalectomized animals, there was an increase in renal HSD2 activity when, along with the HCl overload, the rats were injected with corticosterone. This increment occurred without an increase in enzyme abundance. These results suggest the importance of circulating levels of glucocorticoids to respond to a metabolic acidosis, through regulation of HSD2 stimulation. The group subjected to a simulated gavage showed an increase in enzyme activity and protein abundance, thus demonstrating the need for both adrenal and extra-factors in the modulation of renal HSD2. The adrenalectomized animals injected with different doses of corticosterone, produced a progressive increase in enzyme activity and abundance, being significant for the dose of 68 microg corticosterone/100 g body weight. The highest dose (308 microg/100 g body weight) did not show any variation in activity and abundance compared to the control group. This biphasic effect of glucocorticoids could be explained taking into account their permissive and suppressive actions, depending on their blood levels. Knowing that stress induces multifactorial responses, it should not be surprising to observe a differential regulation in renal HSD2, confirming that different stressors act through different factors of both, adrenal and extra-adrenal origin.     

Adrenal gland involvement in synchronizing the preovulatory release of LH in rats.

In this study we have demonstrated that acute adrenalectomy (1000 hr proestrus) has no effect on the release of LH on proestrous afternoon. However, chronic adrenalectomy results in the loss of some factor responsible for synchronizing the preovulatory LH surge. Since this investigator has shown previously (15) that progesterone can influence the timing of LH release in ovariectomized and ovariectomized-adrenalectomized animals, it is most likely that adrenal progesterone is involved in synchronizing this event.     

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

The mechanisms underlying the onset of obesity are complex and not completely understood. An imbalance of autonomic nervous system has been proposed to be a major cause of great fat deposits accumulation in hypothalamic obesity models. In this work we therefore investigated the adrenal chromaffin cells in monosodium glutamate (MSG)-treated obese female mice. Newborn mice were injected daily with MSG (4 mg/g body weight) or saline (controls) during the first five days of life and studied at 90 days of age. The adrenal catecholamine content was 56.0% lower in the obese group when compared to lean controls (P < 0.0001). Using isolated adrenal medulla we observed no difference in basal catecholamine secretion percentile between obese and lean animals. However, the percentile of catecholamine secretion stimulated by high K+ concentration was lower in the obese group. There was a decrease in the tyrosine hydroxylase enzyme expression (57.3%, P < 0.004) in adrenal glands of obese mice. Interestingly, the expression of dopamine beta-hydroxylase was also reduced (47.0%, P < 0.005). Phenylethanolamine N-methyltransferase expression was not affected. Our results show that in the MSG model, obesity status is associated with a defective adrenal chromaffin cell function. We conclude that in MSG obesity the low total catecholamine content is directly related to a decrease of key catecholamine-synthesizing enzymes, which by its turn may lead to a defective catecholamine secretion.     

Reducing obesity will require involvement of all sectors of society

We need all sectors of society involved in reducing obesity. The food industry's effort to reduce energy intake as part of the Healthy Weight Commitment Foundation is a significant step in the right direction and should be recognized as such by the public health community. We also need to get organizations that promote physical inactivity, such as computer, automobile, and entertainment industries, to become engaged in efforts to reduce obesity.     

Possible involvement of a hypothalamic dopaminergic receptor in development of genetic obesity in mice

We have studied the binding of the dopaminergic agonist 2-[5,8-3H]amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene [( 3H]ADTN) to hypothalamic membranes from the genetically diabetic-obese (db/db) mice and their lean littermates. The specific binding of [3H]ADTN was defined as the difference between the radioligand binding to the membranes in the absence or presence of 1 microM (+)-butaclamol. In order to control nonspecific binding, all binding assays were performed in the presence of 0.1 mM catechol and 0.3 mM ascorbic acid. Binding of [3H]ADTN was rapid, dissociable, saturable and stereoselective. (+)-Butaclamol was very potent whereas (-)-butaclamol was ineffective in inhibiting the binding of this radioligand. Concentration-dependent binding experiments and Scatchard analysis of the data yielded dissociation constant (Kd) of 3.5-4.2 nM and number of binding sites (n) equivalent to 170-200 fmol/mg protein for lean mice. For db/db mice, the data yielded a Kd of 4.0-4.7 nM and an n of 400-500 fmol/mg protein. It was also shown that the anorexic drugs, amphetamine and fenfluramine, inhibited [3H]ADTN binding in a dose-dependent manner. Binding parameters, obtained using membranes from mice made obese by parenteral administration of gold thioglucose, were not significantly different from those obtained for the lean mice. It is concluded that the regulation of the hypothalamic dopaminergic receptors may be related to the lesion in the genetically obese mice.     

Endocannabinoids and liver disease. IV. Endocannabinoid involvement in obesity and hepatic steatosis

Endocannabinoids are endogenous lipid mediators that interact with the same receptors as plant-derived cannabinoids to produce similar biological effects. The well-known appetitive effect of smoking marijuana has prompted inquiries into the possible role of endocannabinoids in the control of food intake and body weight. This brief review surveys recent evidence that endocannabinoids and their receptors are involved at multiple levels in the control of energy homeostasis. Endocannabinoids are orexigenic mediators and are part of the leptin-regulated central neural circuitry that controls energy intake. In addition, they act at multiple peripheral sites including adipose tissue, liver, and skeletal muscle to promote lipogenesis and limit fat elimination. Their complex actions could be viewed as anabolic, increasing energy intake and storage and decreasing energy expenditure, as components of an evolutionarily conserved system that has insured survival under conditions of starvation. In the era of plentiful food and limited physical activity, pharmacological inhibition of endocannabinoid activity offers benefits in the treatment of obesity and its hormonal/metabolic consequences.     

Adrenal cortex disorders in a new model of obesity,Gerbillus gerbillus,exposed to a high carbohydrate diet

Obesity is associated with several endocrine disorders, including hypersensitivity of the hypothalamic-pituitary-adrenal axis. The aim of this study was to investigate the effects of a high carbohydrate diet on structural and ultrastructural features of steroidogenic tissue, as well to evaluate adrenocorticotropic hormone (ACTH), cortisol, and insulin levels in the blood and steroidogenic acute regulatory protein (StAR) expression in the adrenals of gerbils. In electron microscopy, the most pronounced effect of the hypercaloric diet was observed in the zona fasciculata. Plasma levels of ACTH, cortisol, and insulin also showed significant increases. However, no significant change was noted in StAR protein levels. There is evidence that high carbohydrate intake brings about remarkable morphological and functional modifications. This could ultimately lead to mitochondrial alteration and accumulation of lipid droplets, which may lead to inflammation and degeneration of adrenal cells.     

Adrenal Function in Hypothyroidism

In ten patients with hypothyroidism the adrenal response to stimulation with tetracosactrin was found to be normal, and to be unchanged after they had been treated with thyroxine. Though the response to insulin hypoglycaemia was less in the hypothyroid phase, it was never outside the normal limits. Hence it seems unlikely that the adrenal response to stress is appreciably lowered in hypothyroidism.