The pro-opiomelanocortin (POMC) neurons have an anorexigenic action and, when activated, reduce food intake through the release of two peptides, α-melanocyte-stimulating hormone (α-MSH) and cocaine-and-amphetamine-regulated transcripts (CART). The neuropeptide Y (NPY) neurons, on the other hand, release NPY hormone and agouti gene-related protein (AgRP), which prevent the binding of α-MSH to MC3R and MC4R, increasing food intake
This suggests that the central anorexic effects of E2 may occur via ERβ
The main hypothalamic areas involved in food intake and satiety are the arcuate nucleus (ARC), the lateral hypothalamus (LH), the paraventricular nucleus (PVN), the ventromedial hypothalamus (VMH), and the dorsomedial hypothalamus (DMH)
Leptin is a potent anorexigenic and catabolic hormone secreted by adipose cells that reduces food intake and increases energy expenditure
E2 not only modulates leptin receptor mRNA in the ARC and VMH, but also increases hypothalamic sensitivity to leptin, altering peripheral fat distribution
ghrelin. It acts on growth hormone secretagogue receptors (GHSR1a) located in the ARC and is a potent stimulator of food intake
It thus appears that of the two ERs, ERα plays a predominant role in the CNS regulation of lipid and carbohydrate homeostasis.
Both ERs have been identified in the ARC
Stimulation of MCH neurons increases food intake and fat accumulation while its inhibition leads to decreased food intake and reduced fat accumulation.
Both ERs have been identified in the LH
both ERs have been identified in this nucleus
The PVN is the region of the hypothalamus with the highest expression of ERβ and is reported to be weakly ERα positive
The VMH is ERα regulated
Skeletal muscle is responsible for 75% of the insulin-induced glucose uptake in the body
GLUT4 is highly expressed in muscle and represents a rate-limiting step in the insulin-induced glucose uptake
data suggest that in the physiological range, E2 is beneficial for insulin sensitivity, whereas hypo- or hyperestrogenism is related to insulin resistance
In aging female rats, E2 treatment improves glucose homeostasis mainly through its ability to increase muscle GLUT4 content on the cell membrane
It is evident that ERα and ERβ have distinct actions and that much more research is needed to clearly identify the function of each receptor in muscle.
E2 prevents accumulation of visceral fat, increases central sensitivity to leptin, increases the expression of insulin receptors in adipocytes, and decreases the lipogenic activity of lipoprotein lipase in adipose tissue
In rats, ovariectomy increases body weight, intra-abdominal fat, fasting glucose and insulin levels, and insulin resistance followed by decreased phosphorylation of AMPK and its substrate acetyl-CoA carboxylase in adipose tissue
decreased adiponectin, PPARγ coactivator-1α (PGC-1α), and uncoupling protein 2 (UCP2) and increased resistin
Men with aromatase deficiency have truncal obesity, elevated blood lipids, and severe insulin resistance
Although not all studies are in agreement, polymorphisms of ERα in humans have been associated with risk factors for CVDs
Human subcutaneous and visceral adipose tissues express both ERα and ERβ, whereas only ERα mRNA has been identified in brown adipose tissue
suggesting that ERα is the main regulator of GLUT4 expression in adipose tissue
very nice article that looks at the balance of ER-alpha/ER-beta and their role in metabolic syndrome. This article discusses the balance of these receptors are tissue dependent in their effect. I like their conclusion: "...but these mechanisms will never be completely understood if they are not considered in the context of a whole system.
Salivary hormone testing again shown to gold standard. This study looked at salivary cortisol levels in those with Cushing's disease, Cushing's syndrome, and with adrenal incidentaloma. The results make one scratch their head. The sensitivity and specificities of salivary cortisol were very high, exceeding at least 94% with most > 96 and 97%. So, why the opposition? Ignorance I guess.
Probably one of the more disturbing aspects of glyphosate exposure. In utero exposure, lowers Testosterone levels and effects the masculinization process of the young boy. Very disturbing. Our boys are being altered before they are even born.
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it is established that androgen modulates various neurotransmitters in the CNS. Testosterone decreases γ-aminobutyric acid concentration in the hypothalamus, which is blocked by flutamide, a testosterone receptor blocker (14, 15). Testosterone, probably by its conversion to estradiol, increases serotonin transporter mRNA expression in dorsal raphe nucleus (16), and it also increases the density of 5-hydroxytryptamine receptors and serotonin transporter sites in the forebrain (3, 16) of castrated male rats.
very interesting study of 7 men. Increase brain perfusion found and symptom improvement as a result of Testosterone therapy in men ages 58-72. Specific increase perfusion by SPECT scans were in the midbrain and Brodman areas 8 and 24 of the cerebral cortex.
It is now well recognized
that the disease manifestation is reduced in pregnant women with
relapsing-remitting MS
This occurs particularly during the
third trimester when levels of estrogens (estradiol and estriol) and
progesterone (see Table 2) are elevated
up to about 20 times
This seems
well correlated with a decrease in active white matter lesions detected by MRI
This clinical improvement is
however followed by temporary rebound exacerbations at post-partum, when the
hormone levels decline
a shift from Th1 to Th2 immune response, expansion of
suppressive regulatory T lymphocytes and decrease in the number of circulating
CD16+ natural killer (NK)-cells
Th2 cytokines are
associated with down-regulation of Th1 cytokines and this Th2 shift is believed
to provide protection from allograft rejection during pregnancy as well as from
Th1-mediated autoimmune disease
it is
worth noting that the levels of other hormones with anti-inflammatory activity
(1,25-dihydroxy-vitamin D3, norepinephrine, cortisol) also increase
by 2 to 4 times during late pregnancy
1,25-dihydroxy vitamin D3
induces regulatory T-cell function important for development of self-tolerance
breast-feeding does not alter the
relapse rate in women with MS
Leptin is a pleiotropic
hormone produced primarily by adipocytes but also by T lymphocytes and neurons
Several lines of evidence indicate that leptin
contributes to EAE/MS pathogenesis, influencing its onset and clinical severity,
by acting as a proinflammatory cytokine which promotes regulatory T cell (Treg)
anergy and hyporesponsiveness, resulting in increased Th1 (TNFalpha, INFgamma)
and reduced Th2 (IL-4) cytokine production
circulating leptin levels are increased in relapsing-remitting MS
patients (men and women analyzed together) while the
CD4+CD25+Treg population decreases
As the leptin plasma concentrations are
proportional to the amount of fat tissue, obese/overweight individuals produce
higher levels of leptin
Nielsen et al found that estradiol and progesterone exert
neuroprotection against glutamate neurotoxicity, while MPA antagonizes the
neuroprotective effect of estradiol and exacerbated neuron death induced by
glutamate excitotoxicity
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Only abstract available here. The quote that "the toxicity of vitamin E is very low" tells the story. Always have levels evaluated to ensure need. In this review of human studies, doses up to 3,200 IU daily "led to no consistent adverse effects". Also consider the effects of vitamin K effects in those on vitamin E therapy.
could the anti-depressant industry in children and adolescents be a scam? A review of the evidence finds very low quality of evidence with > 56% of the studies being funded by the industry itself; can you say conflict of interest or potential bias? Review finds evidence only that fluoxetine is more effective than placebo in children and adolescents with depression.
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