Melanocortin-4 receptor agonist (RO27-3225) ameliorates soleus but not gastrocnemius atrophy in arthritic rats.

Adjuvant-induced arthritis in rats decreases body weight and muscle mass. Melanocyte stimulating hormone administration to arthritic rats decreases inflammation and skeletal muscle wasting. In this study, we investigate whether activation of melanocortin-4 receptor by RO27-3225 administration is able to prevent the effect of arthritis on the expression of muscle-specific E3 ubiquitin ligases and MyoD in two different muscles, gastrocnemius (a mainly fast type muscle) and soleus (slow type).

Formoterol decreases muscle wasting as well as inflammation in the rat model of rheumatoid arthritis.

Adjuvant-induced arthritis is an experimental model of rheumatoid arthritis that is associated with body weight loss and muscle wasting. β2-adrenergic receptor agonists are powerful anabolic agents that trigger skeletal muscle hypertrophy and have been proposed as a promising treatment for muscle wasting in human patients. The aim of this work was to determine whether formoterol, a selective β2-adrenoreceptor agonist, is able to ameliorate muscle wasting in arthritic rats.

The melanocortin receptor type 3 agonist d-Trp(8)-γMSH decreases inflammation and muscle wasting in arthritic rats.

Background: Chronic inflammatory diseases induce cachexia that increases mortality and morbidity of the illness. Adjuvant-induced arthritis is an experimental model of rheumatoid arthritis that is associated with body weight loss and muscle wasting. Alpha-melanocyte stimulating hormone has an anti-inflammatory effect in arthritic rats and decreases muscle wasting.

Fenofibrate administration to arthritic rats increases adiponectin and leptin and prevents oxidative muscle wasting.

Chronic inflammation induces skeletal muscle wasting and cachexia. In arthritic rats, fenofibrate, a peroxisome proliferator-activated receptor α (PPARα (PPARA)) agonist, reduces wasting of gastrocnemius, a predominantly glycolytic muscle, by decreasing atrogenes and myostatin. Considering that fenofibrate increases fatty acid oxidation, the aim of this study was to elucidate whether fenofibrate is able to prevent the effect of arthritis on serum adipokines and on soleus, a type I muscle in which oxidative metabolism is the dominant source of energy.

Systemic α-melanocyte-stimulating hormone administration decreases arthritis-induced anorexia and muscle wasting.

Rheumatoid cachexia is associated with rheumatoid arthritis and it increases mortality and morbidity. Adjuvant-induced arthritis is an experimental model of rheumatoid arthritis that causes anorexia and muscle wasting. α-Melanocyte-stimulating hormone (α-MSH) has anti-inflammatory actions, and it is able to decrease inflammation in several inflammatory diseases including experimental arthritis.

Effect of cyclooxygenase-2 inhibition by meloxicam, on atrogin-1 and myogenic regulatory factors in skeletal muscle of rats injected with endotoxin.

Cyclooxygenase-2-induction by inflammatory stimuli has been proposed as a mediator of inflammatory cachexia. We analyse whether cyclooxygenase-2 inhibition by meloxicam administration is able to modify the response of skeletal muscle to inflammation induced by lipopolysaccharide endotoxin (LPS). Male rats were injected with 1 mg kg(-1) LPS at 17:00 h and at 10:00 h the following day, and euthanized 4, 24 or 72 hours later.

Fenofibrate, a PPAR{alpha} agonist, decreases atrogenes and myostatin expression and improves arthritis-induced skeletal muscle atrophy.

Arthritis is a chronic inflammatory illness that induces cachexia, which has a direct impact on morbidity and mortality. Fenofibrate, a selective PPARα activator prescribed to treat human dyslipidemia, has been reported to decrease inflammation in rheumatoid arthritis patients. The aim of this study was to elucidate whether fenofibrate is able to ameliorate skeletal muscle wasting in adjuvant-induced arthritis, an experimental model of rheumatoid arthritis.

Application of a low-cost web-based simulation to improve students' practical skills in medical education.

Background: Practical sessions in undergraduate medical education are often costly and have to face constraints in terms of available laboratory time and practice materials (e.g. blood samples from animals).

Leptin impairs insulin signaling in rat adipocytes.

Leptin modulates glucose homeostasis by acting as an insulin-sensitizing factor in most insulin target tissues. Nevertheless, insulin-dependent glucose uptake in white adipose tissue decreases after in vivo treatment with leptin. Moreover, elevated leptin concentrations inhibit insulin metabolic effects in adipocytes.

Long-term food restriction prevents ageing-associated central leptin resistance in wistar rats.

Aims/hypothesis: Ageing is associated with insulin and leptin resistance in mammals. These alterations might be caused by the increased adiposity associated with ageing, by ageing alone or both. We studied whether leptin resistance occurs at the central level in the Wistar rat and we aimed to discriminate between the effects of ageing from those of the increased adiposity associated with ageing.

Decreased leptin uptake in hypothalamic nuclei with ageing in Wistar rats.

Leptin interacts with specific receptors in hypothalamic nuclei and modulates energy balance. Growing evidence has shown the association of obesity and hyperleptinaemia with non-insulin-dependent diabetes mellitus and insulin resistance. The aged Wistar rat shows peripheral insulin resistance in the absence of obesity and alterations of glucose homeostasis.

Gonadal hormones affect neuronal vulnerability to excitotoxin-induced degeneration.

The role of endogenous gonadal secretions in neuroprotection has been assessed in a model of hippocampal degeneration induced by the systemic administration of kainic acid to adult male and female rats. A low dose of kainic acid (7 mg/Kg b.w.

Estrogen uncouples noradrenergic activation of Fos expression in the female rat preoptic area.

The preoptic area of the rat brain is a site at which gonadal steroids act to regulate sexual behaviour and gonadotrophin secretion. The expression of the immediate-early gene product, Fos, in the preoptic area was investigated in conscious ovariectomised, vehicle and estrogen-treated animals which had received an intracerebroventricular (i.c.

Analysis of brainstem A1 and A2 noradrenergic inputs to the preoptic area using microdialysis in the rat.

Noradrenergic inputs to the preoptic area (POA) are involved in regulating a variety of homeostatic functions. However, the accurate measurement of endogenous noradrenaline (NA) release in the POA has been difficult to achieve and consequently little has been done to characterise the different noradrenergic pathways. By combining the technique of intracranial microdialysis with tissue pre-loading of [3H]NA we have developed a sensitive index of NA release in the POA [8].

Controlled neonatal exposure to estrogens: a suitable tool for reproductive aging studies in the female rat.

The present study was designed to determine whether the modification of exposure time to large doses of estrogens provided a reliable model for early changes in reproductive aging. Silastic implants containing estradiol benzoate (EB) in solution were placed into 5-day-old female Wistar rats and removed 1 day (Ei1 group) or 5 days (Ei5) later. In addition, 100 micrograms [corrected] EB dissolved in 100 microliters corn oil was administered s.

Characterization of tritiated noradrenaline release from the rat preoptic area with microdialysis in vivo.

Present techniques are unable to provide a sensitive and accurate index of noradrenergic activity in the rat preoptic area. In this study, we have examined the brainstem A1 noradrenergic input to the preoptic area using a new technique whereby [3H]noradrenaline is preloaded into the preoptic area and release of radioactivity from this region is measured subsequently using microdialysis in vivo. Electrical stimulation of the ipsilateral A1 area for 20 min at 5, 10, and 15 Hz evoked significant increases in dialysate radioactivity that were repeatable and frequency-dependent.

Body weight rhythmicity in the unweaned female rat following neonatal estrogen treatment.

Male and female rats were weighted daily throughout this study to determine whether neonatal exposure to estrogens influences body weight (BW) patterns, particularly during the period before weaning when vaginal opening (VO) occurs as a consequence of this treatment. Females receiving estradiol benzoate (EB) at the age of 5 days had greater body weight than their controls soon after the treatment and until day 21. Clear 3-day periodic changes of BW, between days 9 and 20, were revealed by the spectral analysis of the results in EB-given females which did not occur in their controls.

Luteinizing-hormone-mediated precocious puberty induced in female rats by a prepuberal pituitary graft.

The present study analyzes the mechanism of precocious puberty induced in female rats after a 'young' pituitary graft (obtained from 21-day-old animals). For this purpose, the following experiments have been performed: (1) female rats were grafted or sham-operated on day 21 with a littermate's pituitary the follicle-stimulating hormone (FSH), luteinizing hormone (LH) and estradiol plasma levels as well as the ovarian, uterine and adrenal weights were determined at different times after the graft; (2) female rats grafted or sham-operated on day 21 were treated with 0.2 ml of LH antiserum (LHAS) or the same volume of a normal horse serum (NHS); (3) female rats were injected on day 1 of life with 0.

Effects of neonatal treatment with estrogens on the development of the thymus in rats.

In order to study the effects of sex hormones administered during the neonatal period on the thymic development we have injected 5 days old female rats with a single dose (0.1mg) of estradiol benzoate. The evolution of the thymus gland after treatment was morphometrically analyzed.

Effects of discrete medial preoptic hypothalamic lesions on the androgen gonadotropin feedback system in the male rat.

The effect of discrete lesions of the Anterior Medial Preoptic Area of the Hypothalamus (MPOA) in the control of pituitary gonadotropins in the adult male Wistar rat has been studied. Electrolytic lesions were made by passing an anodal current through tungsten electrodes. Electrodes were oriented stereotaxically into the MPOA and lesion placement was histologically checked.

Effects of the intraventricular administration of 5,7-dihydroxytryptamine on FSH, LH and prolactin secretion in neonatally estrogenized male rats.

The role of the serotoninergic system in the control of LH, FSH and prolactin secretion was analyzed in control and neonatally estrogenized male rats. Animals injected s.c.

[Plasma levels of LH and testosterone in male rats subjected peripheral de-afferentation of the vomeronasal system].

21 day old male rats undergoing peripheral deafferentation of the vomeronasal system (Accessory Olfactory System) show a decrease of the accessory sex organ weight as well as lower LH and testosterone plasmatic levels 30 days later when compared with intact or sham operated rats.

Dissociation of luteinizing hormone and follicle-stimulating hormone control mechanisms in male and female rats by neonatal administration of estradiol benzoate or testosterone propionate.

Testicular atrophy (TA) and decreased plasma luteinizing hormone (LH) levels were observed in the adult male rat after treatment with 500 micrograms of estradiol benzoate (EB) on the first day of life, while administration of 1 mg of testosterone propionate (TP) on the same day was also associated with TA but increased LH levels. TA and no changes in plasma LH levels were seen when the treatment was performed with similar doses of both steroids on day 5 of life. In no case were plasma follicle-stimulating hormone (FSH) levels altered by these treatments.

Oestrogen--bromocriptine interaction in the control of luteinizing hormone and prolactin secretion in the neonatally oestrogenized female rat.

Neonatally oestrogenized female rats showed hyperprolactinaemia (prolactin, 230 micrograms/l), normal LH levels and absence of a positive feedback effect of oestrogen on secretion of LH at 5 months of age. Bromocriptine treatment for 13 days (1 mg/kg per day) caused no changes in LH levels and prolactin levels decreased to normal values (33 micrograms/l). This decrease in prolactin concentration was not followed by the recovery of phasic LH response to oestrogens.

Effect of streptozotocin diabetes on the pituitary-testicular axis in the rat.

The pituitary-testicular axis was investigated in the streptozotocin diabetic male rat to determine the relationship between hormonal alterations and steroidogenic activity. Male Sprague-Dawley rats weighing 250-300 g were used in all experiments. Diabetes was induced by intraperitoneal injection (40 mg/kg body wt.