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Study finds no improvement with glucose control in diabetics.  This study looked at moderately controlled diabetes. Studies have previously shown that poorly controlled diabetes definitely benefits more than those with more mild glucose control problems.  Additionally, the Testosterone levels in this study would not have met the definition of low T by other studies.  So, the question is did these men need T?  Second, did the authors design the study long enough to see changes in the insulin sensitivity and glucose control?  Abstract only available and thus I don't have access to that information.  Third, and this might support the 2nd point, increased lean mass and decreased fat mass was found.  This points to positive metabolic change.  Would this have, given more time, resulted in improved glucose control? No change in visceral adiposity was seen.  This finding, also, is not new.  Testosterone therapy does not improve visceral adiposity.  Though, increasing fat adiposity, low Testosterone, and associated increase in systemic inflammatory cytokine production results in visceral adiposity, Testosterone therapy does reverse the visceral adiposity.  

Study finds that Testosterone regulates glucose metabolism, in part, through adiponectin production.  Early state of low T will slow the use of fats as a source of fuel and this results in an increased energy balance and results in the increased adiponectin production to increase metabolism.  Testosterone and adiponectin exist in an inverse relationship. This study does not mimic normal physiology.  Men with low T are unhealthy with significant metabolic dysfunction.  These young, "healthy" men were induced to a low T state--that is not a clear picture as the physiology of a "young healthy" man is quite different than that of one with low T.   Testosterone conversion to DHT increases GLUT4 and thus glucose uptake--another mechanism of Testosterone's effect on glucose metabolism.

Low Testosterone is a very significant problem in men with type II Diabetes.  Estimated to reach 40%, likely much higher.  They based these estimates only on T levels and sexual symptoms. Testosterone improves glycemic control primarily through Increased transcription and transloction of GLUT4 insulin receptors to the cell surface.  Inflammation reduction is also a mechanism.  Testosteorne lowers Triglycerides in the traditional lipid profile.  Studies are mixed on the other aspects of  lipids.  

Study points to obesity and low Testosterone contribution of neuroinflammation.  No effect of body weight was seen with TRT.  This animal model found similar positive effects of TRT in insulin sensitivity.  Obesity and low T increase inflammatory cytokine production: this study found an increase in TNF-alpha and IL-1beta and TRT reduced TNF-alpha and IL-1beta to near base-line.  Testosterone is neuroprotective and this study reviewed the small volume of evaded that pointed to benefit from estradiol.  Testosterone's effect on glial survival was positive but not significant.  Obesity and low T were found to be associated with increased macrophage infiltration in the PNS with increased TNF-alpha and IL-1beta.   Testosterone therapy improved peripheral neuropathy via its positive effects on nocicieption.

Article discusses the expanding evidence of low T and Metabolic syndrome.

This is the abstract from oral presentation at AACE in Las Vegas from May.  Small study finds reduction in fat mass, increase in muscle mass, increase in insulin sensitivity, and reduction in inflammation signaling with Testosterone therapy in men with low Testosterone.  These men were type 2 diabetics.  This is consistent with prior published literature.  However, men without diabetes, this association is hard to reproduce. The degree of glucose control also effects the response to Testosterone therapy i.e. the worse the glucose control, the more the response from Testosterone.   Also of note, those men with hypogonatrophic hypogonadism had decreased insulin receptor expression, decreased insulin sensitivity, and decreased GLUT-4 expression versus eugonadal men.  Remember from prior studies, it is the conversion of Testosterone to DHT that increases GLUT-4 transcription, translocation, and expression.

Only the abstract available in this publication.  Good study design.  No improvement in insulin resistance, glycemic control or visceral adiposity in obese men with type II diabetes.  The levels of inclusion were TT < 346, which would not meet the criteria put forth by other studies.  This study appeared to look at border line "low T" men with obesity and type II diabetes and found no direct glycemic control improvement.  An increase in lean muscle mass and decrease in subcutaneous fat was found.

Nice discussion of how diet, induces gut bacterial change, that leads to metabolic endotoxemia and disease.

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.

To be read article on Testosterone and Metabolic Syndrome.

Nice review of Testosterone levels and some of the evidence linking Diabetes with low T.  However, the conclusion by the authors regarding what is causing the low T in men with Diabetes is baffling.  The literature does not point to one cause, it is clearly multifactorial--obesity, inflammation, high aromatase activity...I would suggest the authors continue their readings in the manner.

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.

Startling study on the knowledge of Testosterone and cardiovascular disease in general practitioners and cardiologists in Canada.  Eight-eight percent did not screen patients with cardiovascular disease for low Testosterone.  A whopping 67% of physicians did not know that low T was a risk factor for cardiovascular disease, yet 62% believed Testosterone would increase exercise tolerance. The lack of knowledge displayed by physicians today is staggering and is an indictment of the governing bodies.  This was a survey conducted in Canada so there are obvious limitations to the strength/conclusion of this study.

Obesity is associated with low Testosterone and ED in men.