I don't fully understand what this study is saying.
So SHBG increased total T and estrogen and makes it last longer too?
MESO-Rx
Anabolic Steroids
Sex Hormone Binding Globulin [SHBG]
- Thread starter drp90210
- Start date
I don't fully understand what this study is saying.
So SHBG increased total T and estrogen and makes it last longer too?
What are the implications of that for someone on TRT?
Went to a random walk-in doctor today to get a blood work form and she was explaining to me: "Total testosterone doesnt matter its your free testosterone. If you have high SHBG then your testosterone is all bound up by SHBG"
LOL.
I just politely listened and didnt say anything. Just give me the damn lab form lol
But seriously i know that high SHBG is not good but do any doctors acknowledge or know that low SHBG isnt great either???
LOL.
I just politely listened and didnt say anything. Just give me the damn lab form lol
But seriously i know that high SHBG is not good but do any doctors acknowledge or know that low SHBG isnt great either???
De Toni L, Guidolin D, De Filippis V, et al. Osteocalcin and Sex Hormone Binding Globulin Compete on a Specific Binding Site of GPRC6A. Endocrinology 2016;157(11):4473-86. http://press.endocrine.org/doi/10.1210/en.2016-1312?
The undercarboxylated form of osteocalcin (ucOC) regulates male fertility and energy metabolism, acting through the G protein-coupled receptor (GPRC)6A, thus forming a new pancreas-bone-testis axis. Recently, GPRC6A has also been suggested to mediate the nongenomic responses of free testosterone (T).
However, these data did not consider the physiological scenario, where circulating T is mainly bound to sex hormone-binding globulin (SHBG) and only a small percentage circulates freely in the blood.
Here, by the use of computational modelling, we document the existence of similar structural moieties between ucOC and SHBG that are predicted to bind to GPRC6A at docking analysis. This hypothesis of competition was assessed by binding experiments on human embryonic kidney-293 cells transfected with human GPRC6A gene.
Unliganded SHBG specifically bound the membrane of human embryonic kidney-293 cells transfected with GPRC6A and was displaced by ucOC when coincubated at 100-fold molar excess. Furthermore, specific downstream Erk1/2 phosphorylation after stimulation of GPRC6A with ucOC was significantly blunted by 100-fold molar excess of unliganded SHBG.
Intriguingly previous incubation with unliganded SHBG, followed by incubation with T, induced Erk1/2 phosphorylation in a dose-dependent manner. Neither binding nor stimulating activities were shown for SHBG saturated with T.
Experiments on mutation constructs of GPRC6A strengthened the hypothesis of a common binding site of ucOC and SHBG. Given the role of GPRC6A on energy metabolism, these data agree with epidemiological association between SHBG levels and insulin sensitivity, suggest GPRC6A as a likely SHBG receptor, and add bases for the possible regulation of androgen activity in a nonsteroidal manner.
The undercarboxylated form of osteocalcin (ucOC) regulates male fertility and energy metabolism, acting through the G protein-coupled receptor (GPRC)6A, thus forming a new pancreas-bone-testis axis. Recently, GPRC6A has also been suggested to mediate the nongenomic responses of free testosterone (T).
However, these data did not consider the physiological scenario, where circulating T is mainly bound to sex hormone-binding globulin (SHBG) and only a small percentage circulates freely in the blood.
Here, by the use of computational modelling, we document the existence of similar structural moieties between ucOC and SHBG that are predicted to bind to GPRC6A at docking analysis. This hypothesis of competition was assessed by binding experiments on human embryonic kidney-293 cells transfected with human GPRC6A gene.
Unliganded SHBG specifically bound the membrane of human embryonic kidney-293 cells transfected with GPRC6A and was displaced by ucOC when coincubated at 100-fold molar excess. Furthermore, specific downstream Erk1/2 phosphorylation after stimulation of GPRC6A with ucOC was significantly blunted by 100-fold molar excess of unliganded SHBG.
Intriguingly previous incubation with unliganded SHBG, followed by incubation with T, induced Erk1/2 phosphorylation in a dose-dependent manner. Neither binding nor stimulating activities were shown for SHBG saturated with T.
Experiments on mutation constructs of GPRC6A strengthened the hypothesis of a common binding site of ucOC and SHBG. Given the role of GPRC6A on energy metabolism, these data agree with epidemiological association between SHBG levels and insulin sensitivity, suggest GPRC6A as a likely SHBG receptor, and add bases for the possible regulation of androgen activity in a nonsteroidal manner.
Vegan diet is correlated with higher SHBG levels.
Meat eaters: 42.6nmol/L
Vegetarians: 44.6nmol/L
Vegans: 50.9nmol/L
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2374537/pdf/83-6691152a.pdf
Meat eaters: 42.6nmol/L
Vegetarians: 44.6nmol/L
Vegans: 50.9nmol/L
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2374537/pdf/83-6691152a.pdf
SURVEY SEZ.....:
A Vegan diet also happens to correlate even better with being a Weird-Ass biochhhe or faggot-ass MOFO....
LOL
Apologies Tyler but you that VEGAN Crap stroked my Goose the wrong way so now he's gonna HONK...!
BUT - perhaps we are missing something...?
Does the shape of our teeth define our naturally intended diet...?
Sorry Vegans: Here's How Meat-Eating Made Us Human
"If you want a big brain, you'll need more than vegetables -
But sorry, it just ain’t so. As a new study in Nature makes clear, not only did processing and eating meat come naturally to humans, it’s entirely possible that without an early diet that included generous amounts of animal protein, we wouldn’t even have become human—at least not the modern, verbal, intelligent humans we are."
OR
Teeth in Mammals
Canines = Stabbing teeth - normally only 2 pairs (one each side) per jaw. They have a sharp, pointed edge and are used with the incisors to bite into food and or to kill prey. Like incisors they have one root. The tusks of many animals such as elephants are modified canines. They are missing in rodents and most large herbivores (Perissodactyls and Artiodactyls). The gap where the canines would have been is often enlarged and is called a 'diastema'.
A Vegan diet also happens to correlate even better with being a Weird-Ass biochhhe or faggot-ass MOFO....
LOL
Apologies Tyler but you that VEGAN Crap stroked my Goose the wrong way so now he's gonna HONK...!
BUT - perhaps we are missing something...?
Does the shape of our teeth define our naturally intended diet...?
Sorry Vegans: Here's How Meat-Eating Made Us Human
"If you want a big brain, you'll need more than vegetables -
But sorry, it just ain’t so. As a new study in Nature makes clear, not only did processing and eating meat come naturally to humans, it’s entirely possible that without an early diet that included generous amounts of animal protein, we wouldn’t even have become human—at least not the modern, verbal, intelligent humans we are."
OR
Teeth in Mammals
Canines = Stabbing teeth - normally only 2 pairs (one each side) per jaw. They have a sharp, pointed edge and are used with the incisors to bite into food and or to kill prey. Like incisors they have one root. The tusks of many animals such as elephants are modified canines. They are missing in rodents and most large herbivores (Perissodactyls and Artiodactyls). The gap where the canines would have been is often enlarged and is called a 'diastema'.
I was on a partially vegan diet years ago. My SHBG increased from 13 to 19 nmol/L.
One issue with dietary intervention studies is that one usually expects to be able to repeat only the magnitude of change, not the net change. An increase of 8 nmol/L is very significant. However, even the lowest levels in this study are quite high.
The lowest SHBG noted is 42.6 nmol/L. The highest is 50.9 nmol/L. This is an increase of only 16%. If we assume that a vegan diet increases SHBG proportionately to non-diet natural output, and we assume that +16% is the highest magnitude of change we might expect, this would bring a person with SHBG of 13 nmol/L to only 15.08 nmol/L, a net change of 2.08 nmol/L.
One issue with dietary intervention studies is that one usually expects to be able to repeat only the magnitude of change, not the net change. An increase of 8 nmol/L is very significant. However, even the lowest levels in this study are quite high.
The lowest SHBG noted is 42.6 nmol/L. The highest is 50.9 nmol/L. This is an increase of only 16%. If we assume that a vegan diet increases SHBG proportionately to non-diet natural output, and we assume that +16% is the highest magnitude of change we might expect, this would bring a person with SHBG of 13 nmol/L to only 15.08 nmol/L, a net change of 2.08 nmol/L.
Yes. My libido was quite high at the time. I remember it well, as the day of my blood test was my birthday. I had the labs done at that time specifically to see why I was feeling better.
The SHBG increase was a surprise to me, as I was not aware of the dietary link at the time. My vegan diet was loosely followed (but eggs, milk and cheese were fully avoided) and done only for anti-aging purposes. Perhaps if I were strict about it, I could have seen a better result.
I should note that 19 nmol/L is the highest SHBG I've ever had.
Sent from my iPhone using Tapatalk
Off. No TRT.
Do you know of any supplements, food, or drugs that can lower SHBG?
I've heard Aromasin can to some degree, but if you were not on cycle, I'm guessing that taking 25mg/day of Aromasin would crash your Estrogen completely.
I was taking .25mg of Adex every 3 days to keep E2 down. My last test had it at
11.4 pg/mL (8.0 - 35.0). I am now changing Adex dosage to 0.25 every 4 days.
My Total T is currently 839.0 ng/dL (348.0 - 1197.0) and
Free T is at 12.9 pg/mL (8.7 - 25.1).
My DHT is at 27 ng/dL (30 - 85) due to me taking .62mg/day of finasteride for male pattern baldness. So it makes sense that there is more free T available from not converting to DHT.
I'm assuming that SHBG is attaching to my free T and thus not good for someone trying to build muscle or lose fat.
I'd like to be able to do something to free up some more of my T.
Does that make sense?
I've heard Aromasin can to some degree, but if you were not on cycle, I'm guessing that taking 25mg/day of Aromasin would crash your Estrogen completely.
I was taking .25mg of Adex every 3 days to keep E2 down. My last test had it at
11.4 pg/mL (8.0 - 35.0). I am now changing Adex dosage to 0.25 every 4 days.
My Total T is currently 839.0 ng/dL (348.0 - 1197.0) and
Free T is at 12.9 pg/mL (8.7 - 25.1).
My DHT is at 27 ng/dL (30 - 85) due to me taking .62mg/day of finasteride for male pattern baldness. So it makes sense that there is more free T available from not converting to DHT.
I'm assuming that SHBG is attaching to my free T and thus not good for someone trying to build muscle or lose fat.
I'd like to be able to do something to free up some more of my T.
Does that make sense?
Liu S, Sun Q. Sex Differences, Endogenous Sex-hormone Hormones, Sex-hormone Binding Globulin (SHBG), and Exogenous Disruptors in Diabetes and Related Metabolic Outcomes. J Diabetes. Sex Differences, Endogenous Sex‐hormone Hormones, Sex‐hormone Binding Globulin (SHBG), and Exogenous Disruptors in Diabetes and Related Metabolic Outcomes
In assessing clinical and pathophysiological development of type 2 diabetes (T2D), the critical role of the sex steroids axis is underappreciated particularly concerning the sex specific relations with many relevant cardiometabolic outcomes.
In this issue of the Journal, we provide a comprehensive overview of these strong associations of germline variants in the genes governing the sex-steroids pathways, plasma levels of steroid-hormones, and sex hormone-binding globulin (SHBG) with T2D risk that have been observed in many clinical as well as high-quality large prospective cohorts of men and women across ethnic populations.
Taken together, this body of evidence indicates that sex-steroids and SHBG should be routinely incorporated into clinical characterization of T2D patients particularly in screening pre-diabetic patient such as those with the metabolic syndrome using plasma levels of SHBG.
Given that several germline mutations in the SHBG gene have also been directly related to both plasma levels of SHBG and clinical manifestation of T2D, targeting signals in the sex-steroids axis such as SHBG may have significant utility in the prediction and treatment of T2D.
Further, many of the environmental endocrine disrupting chemicals may exert their potential adverse effects on cardiometabolic outcomes via either estrogenic or androgenic signalling pathways, highlighting the importance of using the sex-steroids and SHBG as important biochemical markers in both clinical and population studies in studying sex-specific mechanisms in the pathogenesis of T2D and its complications, as well as the need to equitably allocate resources in studying in both men and women.
In assessing clinical and pathophysiological development of type 2 diabetes (T2D), the critical role of the sex steroids axis is underappreciated particularly concerning the sex specific relations with many relevant cardiometabolic outcomes.
In this issue of the Journal, we provide a comprehensive overview of these strong associations of germline variants in the genes governing the sex-steroids pathways, plasma levels of steroid-hormones, and sex hormone-binding globulin (SHBG) with T2D risk that have been observed in many clinical as well as high-quality large prospective cohorts of men and women across ethnic populations.
Taken together, this body of evidence indicates that sex-steroids and SHBG should be routinely incorporated into clinical characterization of T2D patients particularly in screening pre-diabetic patient such as those with the metabolic syndrome using plasma levels of SHBG.
Given that several germline mutations in the SHBG gene have also been directly related to both plasma levels of SHBG and clinical manifestation of T2D, targeting signals in the sex-steroids axis such as SHBG may have significant utility in the prediction and treatment of T2D.
Further, many of the environmental endocrine disrupting chemicals may exert their potential adverse effects on cardiometabolic outcomes via either estrogenic or androgenic signalling pathways, highlighting the importance of using the sex-steroids and SHBG as important biochemical markers in both clinical and population studies in studying sex-specific mechanisms in the pathogenesis of T2D and its complications, as well as the need to equitably allocate resources in studying in both men and women.
Ring J, Welliver C, Parenteau M, Markwell S, Brannigan RE, Kohler TS. The Utility of Sex Hormone Binding Globulin in Hypogonadism and Infertile Males. J Urol. http://www.jurology.com/article/S0022-5347(17)30021-6/abstract
PURPOSE: We sought to determine what role SHBG played with male infertility patients.
METHODS: Retrospective review of 168 males seen in a fertility clinic from 2012-2014, to investigate the accuracy of TT in the biochemical diagnosis of hypogonadism using cBT as the reference value. We used a multivariable analysis to assess SHBG as an independent predictor of infertility.
RESULTS: Computations using cBT as a standard in the measurement of definitive biochemical hypogonadism (<156 ng/dL) revealed a sensitivity, specificity, PPV, and NPV respectively of 81%, 83%, 81%, and 82% in diagnosing hypogonadism with TT alone.
Of the 90 men with TT >300 ng/dL, 20% had low BT <156 ng/dL, 52% had borderline low BT <210 ng/dL, and only 48% could be considered biochemically eugonadal by cBT. Of the 80 patients with TT <300 ng/dL, 19% had FT levels >6.5ng/dL and thus could be considered to be eugonadal.
SHBG independently predicted by a similar magnitude as FSH decreased sperm concentration (p=.0027) and motility (p=.0447). After excluding men with azoospermia, only SHBG levels differed significantly (p=.0001) in classically hypogonadal men (G1 - TT< 300) and those "missed" but hypogonadal (G2 - cBT < 210). Sperm motility was significantly different in G1 and G2 (p=.014) with more stringent cutoff (cBT < 156).
CONCLUSION: The addition of SHBG to TT serum testing facilitates more accurate diagnosis with FT and cBT with clinical implications of decreased semen parameters to a similar magnitude as FSH, warranting further study of SHBG's role in male infertility.
PURPOSE: We sought to determine what role SHBG played with male infertility patients.
METHODS: Retrospective review of 168 males seen in a fertility clinic from 2012-2014, to investigate the accuracy of TT in the biochemical diagnosis of hypogonadism using cBT as the reference value. We used a multivariable analysis to assess SHBG as an independent predictor of infertility.
RESULTS: Computations using cBT as a standard in the measurement of definitive biochemical hypogonadism (<156 ng/dL) revealed a sensitivity, specificity, PPV, and NPV respectively of 81%, 83%, 81%, and 82% in diagnosing hypogonadism with TT alone.
Of the 90 men with TT >300 ng/dL, 20% had low BT <156 ng/dL, 52% had borderline low BT <210 ng/dL, and only 48% could be considered biochemically eugonadal by cBT. Of the 80 patients with TT <300 ng/dL, 19% had FT levels >6.5ng/dL and thus could be considered to be eugonadal.
SHBG independently predicted by a similar magnitude as FSH decreased sperm concentration (p=.0027) and motility (p=.0447). After excluding men with azoospermia, only SHBG levels differed significantly (p=.0001) in classically hypogonadal men (G1 - TT< 300) and those "missed" but hypogonadal (G2 - cBT < 210). Sperm motility was significantly different in G1 and G2 (p=.014) with more stringent cutoff (cBT < 156).
CONCLUSION: The addition of SHBG to TT serum testing facilitates more accurate diagnosis with FT and cBT with clinical implications of decreased semen parameters to a similar magnitude as FSH, warranting further study of SHBG's role in male infertility.
[OA] Liu CC, Huang SP, Cheng KH, et al. Lower SHBG level is associated with higher leptin and lower adiponectin levels as well as metabolic syndrome, independent of testosterone. Sci Rep 2017;7(1):2727. Lower SHBG level is associated with higher leptin and lower adiponectin levels as well as metabolic syndrome, independent of testosterone
In addition to testosterone (T), the emerging role of sex hormone-binding globulin (SHBG) in pathogenesis of metabolic syndrome (MetS) has been noted recently. However, reports of associations with serum adipocytokine levels are still limited.
Therefore, we conducted this study to evaluate whether serum T and SHBG levels are independent predictors for the risk of MetS that are associated with adiponectin and leptin levels in 614 Taiwanese men over 40 years old collected from a free health screening.
Subjects in the lowest quartile of TT and SHBG levels are exposed to a 1.58 and 3.22 times risk of developing MetS, as compared to those in the highest quartile of TT and SHBG levels. However, SHBG retains its significance independent of TT as a MetS risk predictor, but not vice versa. In addition, SHBG was significantly correlated with both adiponectin and leptin levels even after adjusting for TT levels.
In conclusion, SHBG served as a major predictor for the risk of MetS and was correlated with serum adiponectin and leptin levels that are independent of T. Further studies are needed to elucidate the true role of SHBG in the pathogenesis of MetS and possible mechanisms associated with serum adiponectin and leptin levels.
In addition to testosterone (T), the emerging role of sex hormone-binding globulin (SHBG) in pathogenesis of metabolic syndrome (MetS) has been noted recently. However, reports of associations with serum adipocytokine levels are still limited.
Therefore, we conducted this study to evaluate whether serum T and SHBG levels are independent predictors for the risk of MetS that are associated with adiponectin and leptin levels in 614 Taiwanese men over 40 years old collected from a free health screening.
Subjects in the lowest quartile of TT and SHBG levels are exposed to a 1.58 and 3.22 times risk of developing MetS, as compared to those in the highest quartile of TT and SHBG levels. However, SHBG retains its significance independent of TT as a MetS risk predictor, but not vice versa. In addition, SHBG was significantly correlated with both adiponectin and leptin levels even after adjusting for TT levels.
In conclusion, SHBG served as a major predictor for the risk of MetS and was correlated with serum adiponectin and leptin levels that are independent of T. Further studies are needed to elucidate the true role of SHBG in the pathogenesis of MetS and possible mechanisms associated with serum adiponectin and leptin levels.
I was just about to give you a decent answer until I saw the highlighted text.
Serum Concentrations of Sex Hormone-binding Globulin Vary Widely
BACKGROUND: The testosterone (T) status of a man is influenced by serum concentrations of sex hormone-binding globulin (SHBG). Specifically, tight binding of T to SHBG is believed to render the SHBG-bound T fraction biologically unavailable, meaning that interpretation of T levels in the clinical setting depends in part on knowledge of SHBG concentrations. Although SHBG levels have been reported in population studies, there is scant information for men presenting with clinical symptoms.
OBJECTIVE: To report SHBG values for a large cohort of men presenting to a men's health center.
DESIGN, SETTING, AND PARTICIPANTS: Medical records were reviewed for 1000 consecutive patients seen at our center with a reported SHBG value. SHBG concentrations were measured by a national clinical laboratory using an immunoassay run on a Beckman Coulter DXi system.
OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Patients were age-stratified and data were plotted in the form of comparative histograms.
RESULTS AND LIMITATIONS: The mean age (+/-standard deviation) of the total cohort was 53.5+/-13.5 yr (range 17-91). The mean SHBG was 31.8+/-15.2nmol/l (range 6-109), with a nearly 20-fold difference from the lowest to the highest values. SHBG was >60nmol/l in 5.6% of the men. Patients were stratified according to age. A total of 535 patients were </=54 yr old.
In this younger cohort, the mean age was 40.52+/-7.9 yr (range 17-54) and mean SHBG was 27.7+/-13.3nmol/l (range 6-88), and 2.2% of patients had SHBG >60nmol/l. A total of 465 patients were >/=55 yr old. In this older cohort, the mean age was 64.8+/-7.23 yr (range 55-91) and mean SHBG was 36.6+/-15.8 nmol/l (range 11-109), and 9% of patients had SHBG >60 nmol/l. Mean SHBG was significantly higher in the older group (p<0.001).
CONCLUSIONS: A remarkably wide distribution of SHBG concentrations was observed in a clinical population of men presenting to a men's health center, among both younger and older men. Since SHBG concentrations greatly influence test results for hormones that bind to SHBG, recognition of this large interindividual variability should be considered in the clinical interpretation of these hormone results, particularly for T.
ROUTINE SHBG TESTING SHOULD BE CONSIDERED FOR MEN SUSPECTED OF T DEFICIENCY.
PATIENT SUMMARY: Sex hormone-binding globulin (SHBG) levels vary widely among both older and younger men. This may impact the interpretation of test results for hormones that bind to SHBG, such as testosterone, since the portion that binds to SHBG is believed to not be biologically available.
Krakowsky Y, Conners W, Morgentaler A. Serum Concentrations of Sex Hormone-binding Globulin Vary Widely in Younger and Older Men: Clinical Data from a Men's Health Practice. Eur Urol Focus. http://www.eu-focus.europeanurology.com/article/S2405-4569(17)30126-8/fulltext
BACKGROUND: The testosterone (T) status of a man is influenced by serum concentrations of sex hormone-binding globulin (SHBG). Specifically, tight binding of T to SHBG is believed to render the SHBG-bound T fraction biologically unavailable, meaning that interpretation of T levels in the clinical setting depends in part on knowledge of SHBG concentrations. Although SHBG levels have been reported in population studies, there is scant information for men presenting with clinical symptoms.
OBJECTIVE: To report SHBG values for a large cohort of men presenting to a men's health center.
DESIGN, SETTING, AND PARTICIPANTS: Medical records were reviewed for 1000 consecutive patients seen at our center with a reported SHBG value. SHBG concentrations were measured by a national clinical laboratory using an immunoassay run on a Beckman Coulter DXi system.
OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Patients were age-stratified and data were plotted in the form of comparative histograms.
RESULTS AND LIMITATIONS: The mean age (+/-standard deviation) of the total cohort was 53.5+/-13.5 yr (range 17-91). The mean SHBG was 31.8+/-15.2nmol/l (range 6-109), with a nearly 20-fold difference from the lowest to the highest values. SHBG was >60nmol/l in 5.6% of the men. Patients were stratified according to age. A total of 535 patients were </=54 yr old.
In this younger cohort, the mean age was 40.52+/-7.9 yr (range 17-54) and mean SHBG was 27.7+/-13.3nmol/l (range 6-88), and 2.2% of patients had SHBG >60nmol/l. A total of 465 patients were >/=55 yr old. In this older cohort, the mean age was 64.8+/-7.23 yr (range 55-91) and mean SHBG was 36.6+/-15.8 nmol/l (range 11-109), and 9% of patients had SHBG >60 nmol/l. Mean SHBG was significantly higher in the older group (p<0.001).
CONCLUSIONS: A remarkably wide distribution of SHBG concentrations was observed in a clinical population of men presenting to a men's health center, among both younger and older men. Since SHBG concentrations greatly influence test results for hormones that bind to SHBG, recognition of this large interindividual variability should be considered in the clinical interpretation of these hormone results, particularly for T.
ROUTINE SHBG TESTING SHOULD BE CONSIDERED FOR MEN SUSPECTED OF T DEFICIENCY.
PATIENT SUMMARY: Sex hormone-binding globulin (SHBG) levels vary widely among both older and younger men. This may impact the interpretation of test results for hormones that bind to SHBG, such as testosterone, since the portion that binds to SHBG is believed to not be biologically available.
Krakowsky Y, Conners W, Morgentaler A. Serum Concentrations of Sex Hormone-binding Globulin Vary Widely in Younger and Older Men: Clinical Data from a Men's Health Practice. Eur Urol Focus. http://www.eu-focus.europeanurology.com/article/S2405-4569(17)30126-8/fulltext
Non-Alcoholic Fatty Liver Disease Is an Influencing Factor for The Association of SHBG with Metabolic Syndrome in Diabetes Patients
Metabolic syndrome (MS) and non-alcoholic fatty liver disease (NAFLD) have been identified as risk factors affecting serum sex hormone binding globulin (SHBG) levels. We conducted this cross-sectional study to delineate whether MS or NAFLD has more impact on circulating SHBG levels in type 2 diabetes (T2D) patients. Anthropometric and biochemical parameters including serums SHBG, testosterone (TT), liver enzymes, lipids, insulin, C-peptide and plasma glucose were measured.
Regardless of the MS status, SHBG level was significantly lower in NAFLD patients than in non-NAFLD patients (P < 0.001). In the multiple linear regression analysis, lower serum SHBG level was strongly correlated with a higher incidence of NAFLD, but not MS components.
In logistic regression analyses, after adjusted for age, sex, duration of diabetes, smoking status, and alcohol use, the ORs and 95%CI for presence of MS was 2.26 (95%CI 1.91-2.68) and for presence of NAFLD was 6.36 (95%CI 4.87-8.31) with per one SD decrease in serum SHBG (both P < 0.001).
In conclusion, lower serum SHBG is associated with a higher prevalence of NAFLD, compared with MS and other metabolic disorders, in T2D patients. NAFLD might be an important influencing factor for the association of circulating SHBG with MS in T2D patients.
Hua X, Li M, Pan F, Xiao Y, Cui W, Hu Y. Non-alcoholic fatty liver disease is an influencing factor for the association of SHBG with metabolic syndrome in diabetes patients. Sci Rep 2017;7(1):14532. Non-alcoholic fatty liver disease is an influencing factor for the association of SHBG with metabolic syndrome in diabetes patients
Metabolic syndrome (MS) and non-alcoholic fatty liver disease (NAFLD) have been identified as risk factors affecting serum sex hormone binding globulin (SHBG) levels. We conducted this cross-sectional study to delineate whether MS or NAFLD has more impact on circulating SHBG levels in type 2 diabetes (T2D) patients. Anthropometric and biochemical parameters including serums SHBG, testosterone (TT), liver enzymes, lipids, insulin, C-peptide and plasma glucose were measured.
Regardless of the MS status, SHBG level was significantly lower in NAFLD patients than in non-NAFLD patients (P < 0.001). In the multiple linear regression analysis, lower serum SHBG level was strongly correlated with a higher incidence of NAFLD, but not MS components.
In logistic regression analyses, after adjusted for age, sex, duration of diabetes, smoking status, and alcohol use, the ORs and 95%CI for presence of MS was 2.26 (95%CI 1.91-2.68) and for presence of NAFLD was 6.36 (95%CI 4.87-8.31) with per one SD decrease in serum SHBG (both P < 0.001).
In conclusion, lower serum SHBG is associated with a higher prevalence of NAFLD, compared with MS and other metabolic disorders, in T2D patients. NAFLD might be an important influencing factor for the association of circulating SHBG with MS in T2D patients.
Hua X, Li M, Pan F, Xiao Y, Cui W, Hu Y. Non-alcoholic fatty liver disease is an influencing factor for the association of SHBG with metabolic syndrome in diabetes patients. Sci Rep 2017;7(1):14532. Non-alcoholic fatty liver disease is an influencing factor for the association of SHBG with metabolic syndrome in diabetes patients
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