Fructose upregulates fructokinase activity and this increase liver triglyceride production increasing non-alcoholic fatty liver disease also known as NAFLD.
Elevated uric acid levels up regulate fructose metabolism to triglycerides and fatty liver. This study finds that liver mitochondrial oxidative stress is also evident. This mitochondrial dysfunction also leads to compromised ATP production and fat accumulation specifically through inhibition of aconitase..
low vitamin D associated with an increased odds ratio of elevated blood pressure and elevated triglycerides in post-menopausal women with metabolic syndrome.
Testosterone therapy, undecanoate in this study, found to improve body weight, decrease waist circumference, BMI, lower Total Cholesterol, lower triglycerides, decrease fasting glucose, decrease HgbA1c, decrease blood pressure and increase HDL in men >59.
SHBG positively associated with lower CVD risk profile, CRP, blood pressure, TC, triglycerides..., in young men. This was found independent of Testosterone. This is similar to a lot of the research on Metabolic Syndrome as well.
In some men, Testosterone therapy (10 mg transdermal) is associated with adipose tissue. In those with a decrease in adipose tissue, a decrease in LDL, decrease in Triglycerides, increase in insulin sensitivity, and lower HDL were found.
Waist circumference and triglycerides correlate with serum uric acid levels. Men in this study had higher hyperuricemic rates compared to women. Elevated uric acid levels were associated with increased MetS in both sexes and higher normal uric acid levels were also associated with a higher risk of MetS.
Men with metabolic syndrome have lower Testosterone levels when compared to "healthy" individuals. All men with MetS should have a full androgen analysis performed. This meta-analysis of 20 studies found Testosterone therapy reduced fasting glucose, HOMA, triglycerides, waist circumference by Testosterone in men with MetS. This study found that Testosterone therapy increased HDL as well.
Spice it up for cholesterol. Study finds small, but significant, improvement in in HDL, LDL, and triglycerides with daily curcumin in those with metabolic syndrome.
new study finds Testosterone therapy in men with low T significantly reduces fat, increases lean muscle mass, and reduces fasting glucose and insulin levels. Improvements in total cholesterol, triglycerides and HDL was also seen. Only abstract available currently.
Study finds spore probiotic for 30 days reduced LPS endotoxin by 42%, while the placebo group found a 36% increase. As a result, and to no surprise, there was a significant drop in IL-beta. Also, in the spore probiotic group, there was a 24% reduction in triglycerides.
low carb diet found to benefit atherosclerosis and lipid abnormalities (Triglycerides, HDL, and LDL particle size). Interesting enough, no significant weight loss was seen.
Higher vitamin D levels associated with lower cardio biomarkers: insulin, insulin resistance, triglycerides, TC, LDL and TC:HDL. Not found to be associated: glucose, apoliporotein A1 and B, CRP, fibrinogen, and homocysteine.
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
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
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
Prostate cancer patients with pre-existing T2DM show a further deterioration of insulin resistance and worsening of diabetic
control following ADT
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