T inhibits lipid uptake and lipoprotein-lipase (LDL) activity in adipocytes, and stimulates lipolysis
T inhibits differentiation of adipocyte precursor cells
DHEA stimulates resting metabolic rate (RMR) and lipid oxidation, and enhances glucose disposal, by increasing the expression of GLUT-1 and GLUT-4 on fat cell plasma membrane
The insulin-like effect of DHEA would be associated to a decrease of plasma insulin concentrations and, thus, to an increase of the molar ratio between lipolytic hormones and insulin
the fat-reducing effect of both T and DHEA seems to be more evident at the level of visceral adipose tissue
Testosterone inhibits lipid uptake into adipocytes. Testosterone inhibits lipoprotein lipase. Testosterone stimulated lipolysis. Testosterone inhibits adipocyte differentiation of proginator cells.
DHEAs effects are through different mechanisms.
Both have a preference for activity with visceral adipose tissue.
This study looked at Total serum Testosterone and lipid profiles in men with CAD. What they found is that serum Total Testosterone is positively associated with HDL and negatively associated with LDL.
Testosterone therapy in obese men with type II Diabetes and low T improved weight, lipids, HgbA1c, and blood pressure. There was more improvement with Leptin than with diet/exercise alone.
What is very important is that the control group (diet, exercise, DM meds) had improvement in Testosterone levels, HgbA1c, lipids, BMI, and blood pressure; just not as strong as the treatment arm with Testosterone.
Review article of Curcumin, a polyphenol, reduces insulin resistance, leptin resistance, elevated glucose levels, elevated lipids, and inflammation in obesity and metabolic dysfunction. Adiponectin levels were increased.
good read on an alternate hypothesis of the pathophysiology of MS. THe author proposes that MS is an inflammatory induced dysfunction of lipid metabolism. This is in contrast to the current held dogma that MS is an autoimmune disease.
alpha lipoic acid found to improve insulin sensitivity and reduce oxidative stress and inflammatory markers. In this study, IV ALA was given daily for 2 weeks, and the result was reduced oxidized LDL and all other lipids, improved insulin sensitivity, reduced TNF-alpha, IL-6, and 8-iso-prostaglandin, and increased adiponectin.
TBARS were found elevated in Alzheimer's individuals. TBARS are the result of oxidative stress. Thus TBARS can be used to evaluate lipid peroxidation (oxidative damage) in the brain.
Study finds Testosterone inversely associated with TC, TG, and LDL, but positively associated with HDL. The evidence on Testosterone and lipids are mixed. This study shows positive effects all the way around.
Testosterone therapy in post menopausal women appears to have adverse cardiovascular effects in women. The negative effects were an increase in Pulsatility index and adverse change in lipid profiles. This seemed to counter the positive effects by estrogen. Others have proposed that combination E2 and T therapy hide the negative effects of testosterone on CV health in women.
mice study suggests that increased linoleic acid increases lipid oxidation and increases metabolic rate and muscle performance. The point is that some fat is good. Too much Linoleic acid is pro-inflammatory which would promote adiposity. The key is balance.
he gut microbiota enhances the host’s metabolic capacity for processing nutrients and drugs and modulate the activities of
multiple pathways in a variety of organ systems.
Acquisition of the gut microbiota was associated with rapid increase in body weight (4%) over the first 5 days of
colonization
The colonization process stimulated
glycogenesis in the liver prior to triggering increases in hepatic triglyceride synthesis
modifications of hepatic Cyp8b1 expression and the subsequent alteration of bile acid metabolites
Expression and activity of major drug-metabolizing
enzymes (Cyp3a11 and Cyp2c29) were also significantly stimulated
The gut microbiota (GM) exhibits a relatively low level of diversity compared to those of most soil ecosystems and in humans
it is comprised of usually no more than nine phyla of microorganisms, of which only two are dominant: the Firmicutes and the Bacteroidetes
colonization of a germfree gut was rapid and remarkably stable, establishing within only
a week after first exposure
a study conducted on germfree rats by Nicholls et al. showed that 3 weeks were necessary
to obtain a stabilization and “normalization”
the microbiota status affects
the systemic metabolism of the host, modulating the metabolic fingerprint of topographically remote organs such as the liver
and the kidney
Gut colonization induces a rapid weight gain associated with stimulation of hepatic glycogenesis and triglyceride synthesis
Gut colonization alters bile acid metabolite profiles via modulation of hepatic Cyp8b1 expression
Bile acids are well-known contributors to glucose and lipid metabolism in the liver
GM is known to alter bile metabolism
GM is also known to exert a strong influence on the metabolism of xenobiotics
The effects of gut microbiome are not confined to the gut. They alter bile acid metabolism and thus lipid/glucose metabolism. They alter CYP450 activity. They effect metabolism. They effect the metabolism, and thus effects, of other drugs.