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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.  

New insight to new therapy for Pancreatic cancer.  This article/study does a great job of reviewing the biochemistry by which Graviola works against pancreatic cancer.  Graviola was shown to downregulate HIF-1alpha, NF-kappaB, GLUT1, GLUT4, HKII, and LDHA.  Complex 1 of the electron transport was also inhibited.

Alpha lipoic acid aids insulin action of glucose uptake through its GLUT4 activation.  ALA aids diabetes and other states of hyperglycemia.

Testosterone shown to improve GLUT 4 and IRS-1 expression with low dose short term therapy; in contrast, high dose, prolonged therapy shown to down regulate IRS-1 and GLUT 4 expression.  This shows the importance of using saliva for evaluation versus serum.  Serum testing routinely leads to over treatment with high dosages of testosterone.

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.

Good discussion of Glucose transporters--GLUT.

low Testosterone in mouse model associated with reduction in GLUT4 transcription

Just abstract available, but small study finds men fed high calorie typical in western diets results in GLUT4 inactivation in t think that diet needs a long interval to show effects

Authors propose that exercise increases GLUT4 in those with obesity and type 2 diabetes.

Testosterone increases glucose intake through increased GLUT4 translocation and activity.

Great review article of the increased risk of worsening insulin resistance, glycated hemoglobin, and diabetes risk.  Atorvastatin appears to be the worst culprit.  Mechanism partially through a decrease in GLUT4.

This article discusses there relationship of ER-beta and glucose homeostasis.  In this study, low testosterone was associated with increased ER-beta expression.  This resulted in down regulation of GLUT4 and the result is insulin resistance.

Inflammation causes dysregulation of GLUT4 receptor.  This leads to insulin resistance and associated weight gain.  PPAR gamma plays a role here.

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.

The summary statement of this article says it all: "chronic inflammatory state may induce insulin resistance and endothelial dysfunction..."  Inflammation causes insulin dysfunction. And in fact, we know this to be true.  We know that IL-1B and TNF-alpha stimulated by NF-KappaB actually inhibits insulin action via disruption of the GLUT4 receptor.

Exercise, DHEA, and DHT increased GLUT4 uptake of glucose, increasing glycemic control.

BCAA improve glucose metabolism via, in part, up regulation of GLUT2 receptors in the liver

"Induction of HIF-1α by hypoxia (1% O2) or by CoCl2 was markedly inhibited by ascorbate and loading with physiological levels resulted in almost complete reversal of HIF-1α stabilisation. Gene expression was similarly affected, with VEGF mRNA and GLUT-1 up-regulation being inhibited by ascorbate"

In KRAS + CRC, vitamin C downregulates PDK GLUT1, thereby increasing PD increasing Acetyl CoA production.

Great review of the Hypogonadal-obesity-adipocytokine hypothesis.