IL‐6 increases PSA and androgen receptor expression through a STAT3‐dependent pathway in the absence of androgen in LNCaP cells. Our results agreed with those of an earlier study that indicated that IL‐6 induced expression of the androgen receptor, which up‐regulated PSA promoter activity in the androgen‐independent pathway. Moreover, curcumin blocked stimulation of IL‐6 on the androgen receptor, which attenuated PSA gene expression in a ligand‐independent manner.
quercetin down-regulated the expression of anti-apoptosis protein Bcl-2 and up-regulated the expression of pro-apoptosis protein Bax. Caspase-3 was also activated by quercetin, which started a caspase-3-depended mitochodrial pathway to induce apoptosis. It was also found that quercetin inhibited the expression of the cycloocygenase-2
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effect of time and temperature on the viability of melanoma cell lines and expression of HSP 70 & 90 after brief exposure to hyperthermia. While hyperthermia has multiple mechanisms of action, this paper elucidates two essential benefits of high-dose hyperthermia. First, the study illustrates why high-dose hyperthermia treatments (45°C - 47°C) are so much more effective than the low-dose hyperthermia (39°C - 43°C) produced by commercially available heating devices.
We have known that diet and brain inflammation were linked. This study shows a link between, what they call High energy diet (better known as high calorie, high fat, high carb...), and altered hippocampus brain function.
Progesterone receptor (PR) shown to provide an important anti-inflammatory role in breast cancer in this study. PR shown to increase NF-kappaB inhibitor IkBalpha, shown to inhibit aromatase activity, shown to inhibit COX-2 expression and shown to inhibit HER-2/neu expression.
No surprise, testosterone in men and women have different effects. I just wrote a post on this. Testosterone is positively associated with increased risk of diabetes in women, but inversely with men. That is increased T in women equals increased Diabetes in women; contrast with increased T associated with decreased Diabetes in men.
But the interesting point is SHBG. This study found a strong inverse association between SHBG with diabetes in women when compared to men. Meaning: low SHBG is associated with an increased risk of type II Diabetes. This is at the same time that testosterone is associated with an increased risk.
E2 and the inflammatory adipocytokines tumour necrosis factor α (TNFα) and interleukin 6 (IL6) inhibit hypothalamic production
of GNRH and subsequent release of LH and FSH from the pituitary
Leptin, an adipose-derived hormone with a well-known role
in regulation of body weight and food intake, also induces LH release under normal conditions via stimulation of hypothalamic
GNRH neurons
In human obesity, whereby adipocytes are producing elevated amounts of leptin, the hypothalamic–pituitary axis becomes
leptin resistant
there is evidence from animal studies
that leptin resistance, inflammation and oestrogens inhibit neuronal release of kisspeptin
Beyond hypothalamic action, leptin also directly inhibits the stimulatory action of gonadotrophins on the Leydig cells
of the testis to decrease testosterone production; therefore, elevated leptin levels in obesity may further diminish androgen
status
Prostate cancer patients with pre-existing T2DM show a further deterioration of insulin resistance and worsening of diabetic
control following ADT
ADT for the treatment of prostatic carcinoma in some large epidemiological studies has been shown to be associated with an
increased risk of developing MetS and T2DM
Non-diabetic men undergoing androgen ablation show increased occurrence of new-onset diabetes and demonstrate elevated
insulin levels and worsening glycaemic control
increasing insulin resistance assessed by glucose tolerence test and hypoglycemic clamp was shown to be associated
with a decrease in Leydig cell testosterone secretion in men
The response to testosterone replacement of insulin sensitivity is in part dependent on the androgen receptor (AR)
Low levels of testosterone have been associated with an atherogenic lipoprotein profile, characterised by high LDL and triglyceride
levels
a positive correlation between serum testosterone and HDL has been reported in both healthy and diabetic
men
up to 70% of the body's insulin sensitivity is accounted for by muscle
Testosterone deficiency is associated with a decrease in lean body mass
relative muscle mass is inversely associated
with insulin resistance and pre-diabetes
GLUT4 and IRS1 were up-regulated in cultured adipocytes and skeletal
muscle cells following testosterone treatment at low dose and short-time incubations
local conversion of testosterone to
DHT and activation of AR may be important for glucose uptake
inverse correlation between testosterone levels and adverse mitochondrial function
orchidectomy of male Wistar rats and associated testosterone deficiency induced increased absorption of glucose
from the intestine
(Kelley & Mandarino 2000). Frederiksen et al. (2012a) recently demonstrated that testosterone may influence components of metabolic flexibility as 6 months of transdermal testosterone
treatment in aging men with low–normal bioavailable testosterone levels increased lipid oxidation and decreased glucose oxidation
during the fasting state.
Decreased lipid oxidation coupled with diet-induced chronic FA elevation is linked to increased accumulation of myocellular
lipid, in particular diacylglycerol and/or ceramide in myocytes
In
the Chang human adult liver cell line, insulin receptor mRNA expression was significantly increased following exposure to
testosterone
Testosterone deprivation via castration of male rats led to decreased expression of Glut4 in liver tissue, as well as adipose and muscle
oestrogen was found to increase the expression of insulin receptors in insulin-resistant HepG2 human liver cell
line
FFA decrease hepatic
insulin binding and extraction, increase hepatic gluconeogenesis and increase hepatic insulin resistance.
Only one, albeit large-scale,
population-based cross-sectional study reports an association between low serum testosterone concentrations and hepatic steatosis
in men (Völzke et al. 2010)
This suggests that testosterone may confer some of its beneficial effects on hepatic lipid metabolism via conversion to
E2 and subsequent activation of ERα.
hypogonadal men exhibiting a reduced lean body mass and an increased fat mass, abdominal or central obesity
visceral adipose tissue was inversely correlated with
bioavailable testosterone
there was no change in visceral fat mass in aged men with low testosterone levels
following 6 months of transdermal TRT, yet subcutaneous fat mass was significantly reduced in both the thigh and the abdominal
areas when analysed by MRI (Frederiksen et al. 2012b)
ADT of prostate cancer patients increased both visceral and subcutaneous abdominal fat in a 12-month prospective
observational study (Hamilton et al. 2011)
Catecholamines are the major lipolysis regulating hormones in man and
regulate adipocyte lipolysis through activation of adenylate cyclase to produce cAMP
deficiency of androgen action decreases lipolysis and is primarily
responsible for the induction of obesity (Yanase et al. 2008)
may be some regional differences in the action of testosterone on
subcutaneous and visceral adipose function
proinflammatory adipocytokines IL1, IL6 and TNFα are increased in obesity with a downstream effect that stimulates
liver production of CRP
observational evidence suggests that
IL1β, IL6, TNFα and CRP are inversely associated with serum testosterone levels in patients
TRT has been reported to significantly reduce these proinflammatory mediators
This suggests a role for AR in the metabolic actions of testosterone on fat accumulation and adipose tissue inflammatory
response
testosterone treatment may have beneficial effects on preventing the pathogenesis of obesity by inhibiting adipogenesis,
decreasing triglyceride uptake and storage, increasing lipolysis, influencing lipoprotein content and function and may directly
reduce fat mass and increase muscle mass
Early interventional
studies suggest that TRT in hypogonadal men with T2DM and/or MetS has beneficial effects on lipids, adiposity and parameters
of insulin sensitivity and glucose control
Evidence that whole-body insulin sensitivity is reduced in testosterone deficiency and increases with testosterone replacement
supports a key role of this hormone in glucose and lipid metabolism
Impaired insulin sensitivity in these three tissues is
characterised by defects in insulin-stimulated glucose transport activity, in particular into skeletal muscle, impaired insulin-mediated
inhibition of hepatic glucose production and stimulation of glycogen synthesis in liver, and a reduced ability of insulin
to inhibit lipolysis in adipose tissue
