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.
Serum concentrations of BCAAs are decreased, while the concentrations of the aromatic amino acids (AAAs) phenylalanine and tyrosine are increased, in patients with advanced liver diseases, resulting in a low ratio of BCAAs to AAAs, a ratio called the Fischer ratio
BCAAs were reported to stimulate the production of hepatocyte growth factor
a simplified Fischer ratio, the BCAA to tyrosine ratio (BTR), has been reported useful for predicting serum albumin concentration one year later
BCAA supplementation was shown to delay the progression of CCl4-induced chronic liver injury in a rat model by reducing hepatic apoptosis
BCAAs promoted hepatocyte regeneration in a rat model of hepatectomy
BCAA supplementation for advanced cirrhotic patients improves nutritional status and quality of life
BCAAs activate mTOR and subsequently increase the production of eukaryotic initiation factor 4E-binding protein-1 and ribosomal protein S6 kinase, which upregulate the synthesis of albumin
BCAAs were shown to improve homeostasis model assessment scores for insulin resistance (HOMA-IR) and beta cell function (HOMA-%B) in patients with chronic liver disease, indicating that BCAAs can ameliorate insulin resistance
Several clinical trials have suggested that BCAA supplementation improves the prognosis of cirrhotic patients
A low Fischer ratio has been associated with hepatic encephalopathy
Treatment with BCAAs may therefore have a beneficial effect on patients with hepatic encephalopathy mainly by compensating decreased ratio of BCAAs to AAAs, but not by reducing serum ammonia levels
Two randomized studies also showed that BCAAs did not clearly prevent HE in patients with advanced cirrhosis, although BCAAs prevented the progression of hepatic failure
a systematic review with meta-analyses on the effect of oral BCAAs for the treatment of HE was published[66]. The review has revealed that supplementation of oral BCAAs in cirrhotic patients inhibits the manifestation of HE, especially in patients with overt HE rather than those with minimal HE, but showed no effect on the survival of those patients[66]. Thus, oral administration of BCAAs is the treatment of choice in cirrhotic patients with HE
Exercise is key to healthy lifestyle: High Intensity Interval Training for Insulin resistance found to improve waist circumference, systolic bp, and HOMA-IR; Increased non-responders for insulin and glucose in those with mild IR versus severe IR.
both obesity and low testosterone are linked with promotion of inflammatory pathways [70–72] and exert harmful actions on the central [73–75] and peripheral [29,76] nervous systems
In general, obesity-related changes were worsened by low testosterone and improved by testosterone treatment; however, this relationship was not statistically significant in several instances. Further, our data suggest that a common pathway that may contribute to obesity and testosterone effects is regulation of inflammation
fasting blood glucose levels were independently and additively increased by GDX-induced testosterone depletion and high-fat diet
testosterone treatment significantly reduced fasting glucose under both the normal and high-fat diets, demonstrating potential therapeutic efficacy of testosterone supplementation
fasting insulin, insulin resistance (HOMA index), and glucose tolerance, low testosterone tended to exacerbate and or testosterone treatment improved outcomes.
testosterone status did not significantly affect body weight
testosterone’s effects likely do not indicate an indirect result on adiposity but rather regulatory action(s) on other aspects of metabolic homeostasis
Prior work in rodents has shown diet-induced obesity induces insulin resistance in rat brain [63] and that testosterone replacement improves insulin sensitivity in obese rats [64]. Our findings are consistent with the human literature, which indicates that (i) testosterone levels are inversely correlated to insulin resistance and T2D in healthy [30,65] as well as obese men [66], and (ii) androgen therapy can improve some metabolic measures in overweight men with low testosterone
it has been shown that TNFα has inhibitory effects on neuron survival, differentiation, and neurite outgrowth
Our data demonstrate that low testosterone and obesity independently increased cerebrocortical mRNA levels of both TNFα and IL-1β
Testosterone status also affected metabolic and neural measures
many beneficial effects of testosterone, including inhibition of proinflammatory cytokine expression
neuroprotection [80,81], are dependent upon androgen receptors, the observed effects of testosterone in this study may involve androgen receptor activation
testosterone can be converted by the enzyme aromatase into estradiol, which is also known to exert anti-inflammatory [82] and neuroprotective [83] actions
glia are the primary sources of proinflammatory molecules in the CNS
poorer survival of neurons grown on glia from mice maintained on high-fat diet
Since testosterone can affect glial function [86] and improve neuronal growth and survival [87–89], it was unexpected that testosterone status exhibited rather modest effects on neural health indices with the only significant response being an increase in survival in the testosterone-treated, high-fat diet group
significantly increased expression of TNFα and IL-1β in glia cultures derived from obese mice
testosterone treatment significantly lowered TNFα and IL-1β expression to near basal levels even in obese mice, indicating a protective benefit of testosterone across diet conditions
IL-1β treatment has been shown to induce synapse loss and inhibit differentiation of neurons
Testosterone status and diet-induced obesity were associated with significant regulation of macrophage infiltration
testosterone prevented and/or restored thermal nociception in both diet groups
a possible mechanism by which obesity and testosterone levels may affect the health of both CNS and PNS
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.
Myo-inositol plus diet improved systolic and diastolic blood pressure, HOMA index, cholesterol, and triglyceride serum levels with highly significant differences,
Supplementation with myo-inositol may be considered a reliable option in the treatment of metabolic syndrome in postmenopausal women
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.
there appears to be a positive correlation between serum testosterone levels and insulin sensitivity in men across the full spectrum of glucose tolerance (Pitteloud et al, 2005), and this relationship is at least partially direct and not fully dependent on (changes in) elements of the MetS
supervised D&E alone led to significant improvements in testosterone concentrations, glycemic control, and components of the MetS
diet control, exercise, and testosterone supplementation may be beneficial in the management of men with T2D
androgen-deprivation therapy in males with prostatic cancer may be associated with an increased risk for T2D, which may be caused by negative effects on insulin sensitivity
insulin sensitivity, measured by HOMA, improved in both groups and with a significantly greater degree when testosterone was added to supervised D&E
Fasting insulin concentrations, a good representative of insulin sensitivity, did show a significant correlation with changes in circulating androgen levels, an observation in support of Pitteloud et al (2005), who showed a direct relationship between insulin sensitivity and circulating testosterone concentrations using the hyper-insulinemic euglycemic clamp technique
52 weeks of testosterone treatment also significantly improved circulation levels of adiponectin and hsCRP, key serum markers of insulin sensitivity and hepatic steatosis
The changes in both adiponectin and hsCRP were significantly correlated with the therapy-induced changes in bioavailable testosterone
a negative correlation was found between hsCRP levels and bioavailable testosterone
serum PSA concentrations did not differ between the 2 treatment groups, indicating that short-term testosterone administration appears to be acceptably safe
Study of men with metabolic syndrome and type II Diabetes finds that diet and exercise alone improved glucose control and metabolic syndrome components by 31%. The addition of Testosterone therapy increased this % to 81%.
Data review finds NAC improves pregnancy rates and ovulation rates in women with PCOS against placebo. Meta-analysis revealed limited studies on the topic. When compared to metformin, there was no difference found. Though, one wonders if attacking insulin resistance through proper diet and additional neutraceutical approach would negate that. The reason? NAC and metformin are working in different biochemical pathways. The authors here seem to not realize this. It appears that they think NAC and metormin are both working in the same manner, but they don't. The fact that there is still benefit found compared to placebo, despited the authors lack of understanding of what NAC is and does is a positive.