Omega-3 PUFA metabolism and brain modifications during aging.

In Canada, 5.5 million (16% of Canadians) adults are >65 years old and projections suggest this number will be approximately 20% of Canadians by 2024. A major concern regarding old age is a decline in health, especially if this entails a loss of self-sufficiency and independence caused by a decline in cognition.

Angiotensin II type 2 receptor promotes adipocyte differentiation and restores adipocyte size in high-fat/high-fructose diet-induced insulin resistance in rats.

This study was aimed at establishing whether specific activation of angiotensin II (ANG II) type 2 receptor (AT2R) modulates adipocyte differentiation and function. In primary cultures of subcutaneous (SC) and retroperitoneal (RET) preadipocytes, both AT2R and AT1R were expressed at the mRNA and protein level. Cells were stimulated with ANG II or the AT2R agonist C21/M24, alone or in the presence of the AT1R antagonist losartan or the AT2R antagonist PD123,319.

Presence of task-1 channel in the laryngeal mucosa in the newborn lamb.

Nearly 40 potassium channels have been described in respiratory epithelial cells. Of these are found several members of the 4-transmembrane domain, 2-pore K(+) channel family (K2P family), namely Twik-1 and -2, Trek-1 and -2, Task-2, -3, and -4, Thik-1, and KCNK7. The aim of this study was to verify whether the Twik-related acid-sensitive K(+) channel, subtype 1 (Task-1) (also known as KCNK3), is present in the laryngeal mucosa in the newborn lamb.

Fyn is involved in angiotensin II type 2 receptor-induced neurite outgrowth, but not in p42/p44mapk in NG108-15 cells.

In NG108-15 cells, activation of p42/p44(mapk) is essential for induction of neurite outgrowth by angiotensin II (Ang II) type 2 receptor (AT(2)). The aim was to verify whether Fyn, a member of the Src family kinases (SFK), is involved in neurite outgrowth induced by AT(2) activation. Preincubation of cells with PP1, a general inhibitor of the SKF, decreased activation of Rap1 and p42/p44(mapk) and abolished TrkA activation by Ang II or by the AT(2) agonist, CGP42112A.

Inhibition of DHCR24/seladin-1 impairs cellular homeostasis in prostate cancer.

Background: Seladin-1 belongs to a subgroup of androgen-dependent genes associated with anti-proliferative, pro-differentiation, and pro-apoptotic functions and plays a protective role against oncogenic stress. The present study aims to investigate the localization and expression of Seladin-1 protein in normal and tumoral human prostatic tissues as well as to explore its role in proliferation and steroid secretion in androgen-dependent (LnCaP) and androgen-independent (DU145) cell lines and in human prostate primary cell culture.

Methods: Seladin-1 protein localization and expression were assessed on whole tissue sections by tissue array/immunohistochemistry and following immunofluorescence and Western blotting.

24-dehydrocholesterol reductase/seladin-1: a key protein differentially involved in adrenocorticotropin effects observed in human and rat adrenal cortex.

DHCR24 (24-dehydrocholesterol reductase), or seladin-1, is one of the most expressed genes in the adrenal gland. Because the rat and human adult adrenal cortex differ in their respective functional properties, the aim of the present study was to verify whether seladin-1 may be differentially involved in basal and ACTH-stimulated steroidogenesis and oxidative stress management. Seladin-1 expression was predominantly observed in both human and rat zona fasciculata, with a predominant cytoplasmic localization in human cells and a nucleo-cytoplasmic distribution in rat cells.

From integrative signalling to metabolic disorders.

The adrenal cortex undergoes constant dynamic structural changes, a key element in ensuring integrative functionality of the gland. Studies have shown that the cellular environment can modulate cell functions such as proliferation and steroid secretion. For example, 3-day treatment with angiotensin II promotes protein synthesis with a concomitant decrease in proliferation of glomerulosa cells, when cultured on fibronectin, but not on collagen IV or laminin.

Angiotensin II type 2 receptor stimulation increases the rate of NG108-15 cell migration via actin depolymerization.

Angiotensin II (Ang II) has been reported to induce migration in neuronal cell types. Using time-lapse microscopy, we show here that Ang II induces acceleration in NG108-15 cell migration. This effect was antagonized by PD123319, a selective AT2 receptor antagonist, but not by DUP753, a selective AT1 receptor antagonist, and was mimicked by the specific AT2 receptor agonist CGP42112.

Adrenocortical dysregulation as a major player in insulin resistance and onset of obesity.

The aim of this review is to explore the dysregulation of adrenocortical secretions as a major contributor in the development of obesity and insulin resistance. Disturbance of adipose tissue physiology is one of the primary events in the development of pathologies associated with the metabolic syndrome, such as obesity and type 2 diabetes. Several studies indicate that alterations in metabolism of glucocorticoids (GC) and androgens, as well as aldosterone in excess, are involved in the emergence of metabolic syndrome.

Seladin-1 expression in rat adrenal gland: effect of adrenocorticotropic hormone treatment.

Seladin-1 (KIAA0018) gene is the seventh most highlyexpressed gene in the adult adrenal gland, along with genes coding for steroidogenic enzymes. The aim of the present study was to investigate the localization of the Seladin-1 protein in control and ACTH-treated rat adrenal glands and to verify whether Seladin-1 is involved in secretion. Immunofluorescence studies revealed that Seladin-1 was localized principally in the zona fasciculata, cytoplasm, and nucleus.

Direct inhibitory effects of leptin on the neonatal adrenal and potential consequences for brain glucocorticoid feedback.

Leptin is most studied for its primary role in the CNS control of energy balance and food intake in humans and rodents, yet it has functions on multiple target sites including the adrenal gland. In adult rodents, leptin has been shown to inhibit adrenal steroidogenesis and we have recently demonstrated that some of the mechanisms responsible for leptin-induced inhibition of adrenal glucocorticoid production, namely a reduction of StAR protein expression are already present in the neonatal adrenal gland. The effect of leptin on the neonatal adrenal gland integrates well with the previously demonstrated effect of this protein to inhibit stress responses, enhance glucocorticoid receptor expression in the CNS and sensitivity to glucocorticoid inhibitory feedback in neonates.

Inhibition of steroidogenic response to adrenocorticotropin by leptin: implications for the adrenal response to maternal separation in neonatal rats.

Previous studies have shown that leptin can regulate the adrenocortical axis. Neonatal rodents exhibit a period of adrenal hyporesponsiveness to stress in the first 2 wk of life, and we determined the role of leptin as a mediator of this process. We examined the direct effects of leptin on neonatal adrenal steroidogenic responses to ACTH under basal conditions and after 24-h maternal separation.

Isolation of differentially expressed genes in conceptuses and endometrial tissue of sows in early gestation.

The implantation period is a critical time for embryonic survival in pigs. During this period, numerous growth factors are secreted by the conceptuses and the uterine endometrium in order to establish pregnancy and to provide a proper environment for embryonic development. It is well known that the Chinese Meishan sows have a larger litter size when compared with occidental sows mainly because of a superior embryonic survival rate.