Impact of cigarette smoke and aerobic physical training on histological and molecular markers of prostate health in rats.

Recent evidence suggests that aerobic physical training may attenuate the deleterious effects of cancer risk factors, including smoking. We investigated the effects of cigarette smoke inhalation and aerobic physical training on the expression of steroid receptors and inflammatory and apoptotic proteins in the prostate. Forty male Wistar rats were distributed in four groups: control (CO), exercise (EXE), cigarette smoke exposure (CS), and cigarette smoke exposure with exercise (CS+EXE). For eight weeks, animals were repeatedly exposed to cigarette smoke for 30 min or performed aerobic physical training either with or without the cigarette smoke inhalation protocol. Following these experiments, we analyzed prostate epithelial morphology and prostatic expression of androgen (AR) and glucocorticoid receptors (GR), insulin-like growth factor (IGF-1), B-cell lymphoma-2 (BCL-2), BCL-2-associated X protein (BAX), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and nuclear factor-kappa B (NF-κB) via immunohistochemistry. Cigarette smoke exposure stimulated the expression of AR, IGF-1, BCL-2, and NF-κB while downregulating BAX, IL-6, and TNF-α labeling in the prostate. In contrast, aerobic physical training attenuated cigarette smoke-induced changes in AR, GR, IGF-1, BCL-2, IL-6, TNF-α, and NF-κB. This suggests that cigarette smoke stimulates inflammation and reduces apoptosis, culminating in increased prostatic epithelial and extracellular matrices, whereas physical training promoted beneficial effects towards maintaining normal prostate morphology and protein levels.

Impact of cigarette smoke and aerobic physical training on histological and molecular markers of prostate health in rats

Recent evidence suggests that aerobic physical training may attenuate the deleterious effects of cancer risk factors, including smoking. We investigated the effects of cigarette smoke inhalation and aerobic physical training on the expression of steroid receptors and inflammatory and apoptotic proteins in the prostate. Forty male Wistar rats were distributed in four groups: control (CO), exercise (EXE), cigarette smoke exposure (CS), and cigarette smoke exposure with exercise (CS+EXE). For eight weeks, animals were repeatedly exposed to cigarette smoke for 30 min or performed aerobic physical training either with or without the cigarette smoke inhalation protocol. Following these experiments, we analyzed prostate epithelial morphology and prostatic expression of androgen (AR) and glucocorticoid receptors (GR), insulin-like growth factor (IGF-1), B-cell lymphoma-2 (BCL-2), BCL-2-associated X protein (BAX), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and nuclear factor-kappa B (NF-κB) via immunohistochemistry. Cigarette smoke exposure stimulated the expression of AR, IGF-1, BCL-2, and NF-κB while downregulating BAX, IL-6, and TNF-α labeling in the prostate. In contrast, aerobic physical training attenuated cigarette smoke-induced changes in AR, GR, IGF-1, BCL-2, IL-6, TNF-α, and NF-κB. This suggests that cigarette smoke stimulates inflammation and reduces apoptosis, culminating in increased prostatic epithelial and extracellular matrices, whereas physical training promoted beneficial effects towards maintaining normal prostate morphology and protein levels.

The effects of lesions of the thalamic intergeniculate leaflet on the pineal metabolism.

The aim of the present work was to study, in rats, the effects of lesions of the thalamic intergeniculate leaflet (IGL) and the deep pineal/lamina intercalaris region (DP) on the diurnal profile of N-acetylserotonin (NAS) and on the nocturnal pineal reactivity to acute retinal light stimulation (1 or 15 min). The 24-h experiment shows that there is no phase-shifting on the diurnal NAS curve of groups of rats with bilateral IGL lesion compared to the controls. On the other hand there is a significant reduction on the amplitude of pineal NAS content observed in every nocturnal point of the curve. The pineal glands of IGL-lesioned rats, after 1 min of retinal light stimulation, keep their NAS content equal to the lesioned dark-killed rats. Nonetheless, after 15 min of photostimulation, the pineal NAS content is reduced to nearly zero equally to the control animals. DP lesion does not modify the content of NAS in the pineal gland of rats killed in the dark. However, the pineal photo-inhibition process induced by 1 min of light exposure is impaired. These results suggest that: (1) the intergeniculate leaflet has a role in regulating the amplitude of the diurnal rhythm of pineal NAS production rather than its phase entrainment to light-dark cycle. This effect is not dependent on the direct geniculo-pineal connections. (2) The nocturnal pineal photo-inhibition phenomenon could be decomposed in two processes. One, triggered by short pulses of light and totally dependent on the IGL and partially dependent on the direct monosynaptic pathway between this structure and the pineal gland.(ABSTRACT TRUNCATED AT 250 WORDS)

GLUT4 protein expression in obese and lean 12-month-old rats: insights from different types of data analysis.

GLUT4 protein expression in white adipose tissue (WAT) and skeletal muscle (SM) was investigated in 2-month-old, 12-month-old spontaneously obese or 12-month-old calorie-restricted lean Wistar rats, by considering different parameters of analysis, such as tissue and body weight, and total protein yield of the tissue. In WAT, an approximately 70% decrease was observed in plasma membrane and microsomal GLUT4 protein, expressed as microg protein or g tissue, in both 12-month-old obese and 12-month-old lean rats compared to 2-month-old rats. However, when plasma membrane and microsomal GLUT4 tissue contents were expressed as g body weight, they were the same. In SM, GLUT4 protein content, expressed as microg protein, was similar in 2-month-old and 12-month-old obese rats, whereas it was reduced in 12-month-old obese rats, when expressed as g tissue or g body weight, which may play an important role in insulin resistance. Weight loss did not change the SM GLUT4 content. These results show that altered insulin sensitivity is accompanied by modulation of GLUT4 protein expression. However, the true role of WAT and SM GLUT4 contents in whole-body or tissue insulin sensitivity should be determined considering not only GLUT4 protein expression, but also the strong morphostructural changes in these tissues, which require different types of data analysis.

Loss of weight restores GLUT 4 content in insulin-sensitive tissues of monosodium glutamate-treated obese mice.

OBJECTIVE: To investigate the effect of weight loss on GLUT 4 content of insulin sensitive tissues of obese mice. SUBJECTS: Mice were made obese by neonatal treatment with monosodium glutamate (MSG). In addition, one group of obese animals was submitted to a caloric restriction to promote 20% weight loss (MSG-L). Both groups were compared to age-matched control mice. MEASUREMENTS: Anthropometric data, glycaemia and insulinaemia were measured. The GLUT 4 protein was assessed by Western blotting analysis in white (WAT) and brown (BAT) adipose tissue, and skeletal (SM) and cardiac (CM) muscles. RESULTS: The MSG mice were very obese according to their morphometric analysis, showing moderate hyperglycaemia with severe hyperinsulinaemia, and reduced (P < 0.001) glucose/insulin (G/I) ratio. The procedure for weight loss promoted a significant (P < 0.001) reduction of both glycaemic and insulinaemic levels, and an increase in G/I ratio. Compared to control animals, the GLUT 4 content in obese MSG mice, was decreased by 30% (P < 0.05) in SM and CM, by 80% (P < 0.001) in BAT and in different subcellular membrane fractions of WAT. On the other hand, transporter protein content was restored to normal levels in MSG-L animals. CONCLUSION: The reduced GLUT 4 content of insulin sensitive tissues from MSG-treated obese mice is recovered by a 20% loss in weight. This mechanism can be involved in the observed increase of insulin sensitivity.

Pinealectomy causes glucose intolerance and decreases adipose cell responsiveness to insulin in rats.

Although the pineal gland influences several physiological systems, only a few studies have investigated its role in the intermediary metabolism. In the present study, male Wistar rats, pinealectomized or sham-operated 6 wk before the experiment, were submitted to both intravenous glucose tolerance tests (IVGTT) and insulin binding as well as glucose transport assays in isolated adipocytes. The insulin receptor tyrosine kinase activity was assessed in liver and muscle. The insulin secretory response during the IVGTT was impaired, particularly in the afternoon, and the glucose transport responsiveness was 33% lower in pinealectomized rats. However, no difference was observed in the insulin receptor number of adipocytes between groups as well as in insulin-stimulated tyrosine kinase activity, indicating that the initial steps in the insulin signaling were well conserved. Conversely, a 40% reduction in adipose tissue GLUT-4 content was detected. In conclusion, pinealectomy is responsible for both impaired insulin secretion and action, emphasizing the influence of the pineal gland on glucose metabolism.