Increased Insulin Resistance Research Articles

(297) Evaluation of Endothelial Function and Metabolic Profile in Patients with Prostate Cancer Undergoing Androgen Deprivation Therapy

Abstract Introduction Androgen deprivation therapy (ADT) has been the cornerstone of prostate cancer treatment. ADT delays cancer progression, alleviates cancer-related symptoms, and is associated with survival gains. Despite these established benefits, the therapy comes with known side effects, such as increased cardiovascular adverse events and metabolic changes. Despite the well-established association between the level of circulating testosterone and endothelial integrity, the direct effects of ADT on endothelial function remain controversial. Objective The aim of the present study was to investigate the impact of ADT on endothelial function, through the analysis of vascular parameters of the brachial artery, and the measurement of serum inflammatory markers. It was also our goal to evaluate early impact of ADT on anthropometric and metabolic parameters Methods We prospectively evaluated men with moderate to high-risk prostate cancer treated with ADT from January to July 2022 at our institution. Patients with decompensated diabetes mellitus (HbA1c >9%), active smokers or smokers who have ceased for less than 5 years and those with confirmed diagnosis of peripheral artery disease, coronary artery disease, angina, congestive heart failure, myocardial infarction, coronary revascularization or stroke, were excluded. Brachial artery assessment included vascular diameter and flow-mediated (endothelium-dependent) vasodilation (FMD) using high-resolution B-mode ultrasound. Our metabolic and inflammatory profile included serum measurement of total cholesterol and fractions, triglycerides, fasting glucose, glycated hemoglobin, basal insulin, C-reactive protein, and bioimpedance assessment of body fat distribution. All measurements were performed at baseline and after 3 months of ADT initiation with goserelin acetate 10.80mg. Results A total of 14 men with mean age of 67.9 ± 6.9 years were included. The prevalence of diabetes in the present cohort was 21.4%. FMD demonstrated a slight increase following ADT, which did not reach statistical significance after 3 months (median 2.2% vs. 5.0%; p = 0.8224 – Figure 1). Baseline brachial artery diameter significantly decreased with ADT compared to baseline (median diameter 0.43cm vs 0.40cm; p = 0.006). With regard to the metabolic profile, ADT significantly increased insulin resistance: fasting insulin levels (mean 9.67 ± 6.09 vs 13.19 ± 7.47; p = 0.002), glycated hemoglobin (mean 5.79% ± 0.47 vs 6.22% ± 0.75; p = 0.009) and homeostatic model assessment insulin resistance increased significantly after 3 months (p = 0.006). Low-density lipoprotein cholesterol (mean 112.00 ± 27.35 vs 128.90 ± 29.00; p = 0.01) and triglycerides (mean 145.40 ± 78.52 vs 168.20 ± 105.80; p = 0.03) concentrations were higher after 3 months of ADT. No significant differences were found in body fat distribution. Conclusions Although the present study has not demonstrated a significant change in brachial artery FMD, we verified an important and surprisingly early worsening of the metabolic profile with ADT, especially increased insulin resistance and dyslipidemia, which represent well-established risk factors for cardiovascular events. Disclosure No

Diabetes, Diabetic Retinopathy, and Inflammatory Disorders

ABSTRACT This review summarizes the impact of systemic and ocular inflammatory disorders on diabetes mellitus (DM) and diabetic retinopathy (DR). Local inflammation is a key pathology in diabetic retinopathy (DR) and is also an evolving target for clinical therapy. The legacy effects of local inflammation at the intracellular level make DR a persistent self-driven vicious process. Ocular inflammation is accompanied as well as incited by systemic inflammation due to diabetes mellitus (DM) itself. Over the years, a multitude of studies have evaluated the impact of systemic inflammatory disorders (SIDs, like rheumatoid arthritis, lupus, psoriasis, etc.) and anti-inflammatory drugs prescribed for managing them on manifestations of DM. Recent studies have indicated increased insulin resistance to be a result of chronic inflammation, and the anti-inflammatory drugs to have a protective effect towards DM. Very few studies have evaluated the impact of SIDs on DR. Furthermore, the evidence from these studies is conflicting, and while local anti-inflammatory therapy has shown a lot of clinical potential for use in DR, the results of systemic anti-inflammatory therapies have been inconsistent. The impact of local ocular inflammation due to uveitis on DR is a crucial aspect that has not been evaluated well at present. Initial pre-clinical studies and small-sized clinical reports have shown a strong and positive relationship between the presence of uveitis and the severity of DR as well as its progression, while larger cross-sectional patient surveys have refuted the same. The long term impact of ocular inflammation due to uveitis on DR needs to be studied while adjusting for confounders.

Effect of High Fat Diet on Disease Development of Polycystic Ovary Syndrome and Lifestyle Intervention Strategies.

Polycystic ovary syndrome (PCOS) is a prevalent endocrine and metabolic disorder that affects premenopausal women. The etiology of PCOS is multifaceted, involving various genetic and epigenetic factors, hypothalamic-pituitary-ovarian dysfunction, androgen excess, insulin resistance, and adipose-related mechanisms. High-fat diets (HFDs) has been linked to the development of metabolic disorders and weight gain, exacerbating obesity and impairing the function of the hypothalamic-pituitary-ovarian axis. This results in increased insulin resistance, hyperinsulinemia, and the release of inflammatory adipokines, leading to heightened fat synthesis and reduced fat breakdown, thereby worsening the metabolic and reproductive consequences of PCOS. Effective management of PCOS requires lifestyle interventions such as dietary modifications, weight loss, physical activity, and psychological well-being, as well as medical or surgical interventions in some cases. This article systematically examines the pathological basis of PCOS and the influence of HFDs on its development, with the aim of raising awareness of the connection between diet and reproductive health, providing a robust approach to lifestyle interventions, and serving as a reference for the development of targeted drug treatments.

Beta Cell Dysfunction in Youth- and Adult-Onset Type 2 Diabetes: An Extensive Narrative Review with a Special Focus on the Role of Nutrients.

Traditionally a disease of adults, type 2 diabetes (T2D) has been increasingly diagnosed in youth, particularly among adolescents and young adults of minority ethnic groups. Especially, during the recent COVID-19 pandemic, obesity and prediabetes have surged not only in minority ethnic groups but also in the general population, further raising T2D risk. Regarding its pathogenesis, a gradually increasing insulin resistance due to central adiposity combined with a progressively defective β-cell function are the main culprits. Especially in youth-onset T2D, a rapid β-cell activity decline has been observed, leading to higher treatment failure rates, and early complications. In addition, it is well established that both the quantity and quality of food ingested by individuals play a key role in T2D pathogenesis. A chronic imbalance between caloric intake and expenditure together with impaired micronutrient intake can lead to obesity and insulin resistance on one hand, and β-cell failure and defective insulin production on the other. This review summarizes our evolving understanding of the pathophysiological mechanisms involved in defective insulin secretion by the pancreatic islets in youth- and adult-onset T2D and, further, of the role various micronutrients play in these pathomechanisms. This knowledge is essential if we are to curtail the serious long-term complications of T2D both in pediatric and adult populations.

The Presence of Periodontitis Exacerbates Non-Alcoholic Fatty Liver Disease via Sphingolipid Metabolism-Associated Insulin Resistance and Hepatic Inflammation in Mice with Metabolic Syndrome.

Clinical studies have shown that periodontitis is associated with non-alcoholic fatty liver disease (NAFLD). However, it remains unclear if periodontitis contributes to the progression of NAFLD. In this study, we generated a mouse model with high-fat diet (HFD)-induced metabolic syndrome (MetS) and NAFLD and oral P. gingivalis inoculation-induced periodontitis. Results showed that the presence of periodontitis increased insulin resistance and hepatic inflammation and exacerbated the progression of NAFLD. To determine the role of sphingolipid metabolism in the association between NAFLD and periodontitis, we also treated mice with imipramine, an inhibitor of acid sphingomyelinase (ASMase), and demonstrated that imipramine treatment significantly alleviated insulin resistance and hepatic inflammation, and improved NAFLD. Studies performed in vitro showed that lipopolysaccharide (LPS) and palmitic acid (PA), a major saturated fatty acid associated with MetS and NAFLD, synergistically increased the production of ceramide, a bioactive sphingolipid involved in NAFLD progression in macrophages but imipramine effectively reversed the ceramide production stimulated by LPS and PA. Taken together, this study showed for the first time that the presence of periodontitis contributed to the progression of NAFLD, likely due to alterations in sphingolipid metabolism that led to exacerbated insulin resistance and hepatic inflammation. This study also showed that targeting ASMase with imipramine improves NAFLD by reducing insulin resistance and hepatic inflammation.

Deficiency of S100 calcium binding protein A9 attenuates vascular dysfunction in aged mice

BackgroundS100 calcium-binding protein A9 (S100A9) is a danger-associated molecular pattern molecule that mediates the inflammatory response. Inflammation is essential in aging-related cardiovascular diseases. However, less is known regarding the role of S100A9 in vascular aging. MethodsS100A9 null mice were used to investigate the role of S100A9 in aging-related pathologies. Artery rings were used to measure the functional characteristics of vascular with a pressurized myograph. Telomere length, Sirtuin activity, oxidative stress, and endothelial nitric oxide synthetase (eNOS) activity were used to elevate vascular senescence. Intraperitoneal glucose tolerance (IPGTT) and insulin sensitivity test (IST) were employed to investigate the effects of S100A9 on insulin resistance. Inflammation response was reflected by the concentration of inflammatory cytokines. The Toll-like receptor 4 (TLR4) and receptor for advanced glycation end products (RAGE) inhibitors were used to identify the downstream molecular mechanisms of S100A9 in aging-induced senescence in endothelial cells. ResultsS100A9 expression in vascular increased with aging in mice and humans. Deficiency of S100A9 alleviated vascular senescence in aged mice, as evidenced by increased telomere length, Sirtuin activity, and eNOS activity. Meanwhile, S100A9 knockout improved endothelium-dependent vasodilatation and endothelial continuity in aged mice. Moreover, the increased insulin resistance, oxidative stress, and inflammation were mitigated by S100A9 deletion in aged mice. In vitro, S100A9 induced senescence in endothelial cells, and that effect was blunted by TLR4 but not RAGE inhibitors. ConclusionThe present study suggested that S100A9 may contribute to aging-related pathologies and endothelial dysfunction via the TLR4 pathway. Therefore, targeting S100A9/TLR4 signaling pathway may represent a crucial therapeutic strategy to prevent age-related cardiovascular diseases.

Does increasing insulin resistance in adolescence actively decrease cerebral perfusion to oral glucose tolerance test?

Background: Approximately 20% of American adolescents are obese, and nearly half demonstrate some form of insulin resistance (IR). Insulin acts as a metabolic hormone, a neurotrophic growth factor, and a vasodilator. Notably, adults with neurologic disease often exhibit IR and reduced cerebral blood flow (CBF). Adolescent brains are actively growing such that IR may negatively impact brain health in part due to lower brain perfusion. Specifically, given the role of insulin as a potential vasodilator, we hypothesized CBF would increase in response to a physiologic glucose-insulin surge, but this effect would lessen as IR level increased. Methods: Adolescents (n=11, 3 females, age=14.8±2 yr, BMI=24.7±7) taking no medications were studied. IR was estimated by calculating HOMA-IR using fasting glucose and insulin, spanning a spectrum of IR (excluding diabetes). Subjects completed a magnetic resonance imaging (MRI) study visit to assess cerebral perfusion using arterial spin labeling (ASL). Heart rate (HR), mean arterial pressure (MAP) and end tidal CO 2 (ETCO 2 ) were assessed at baseline and during oral glucose tolerance test (OGTT); ingesting 75g glucose in 296mL water (Trutol). Venous blood was sampled at baseline and 5, 10, 20, 30, 45, and 60 minutes post OGTT. Perfusion at peak plasma insulin was compared to baseline. Significance was determined using linear regression of change in perfusion (peak- baseline) versus HOMA-IR and set at p≤0.05. Results: Results are mean±SD. HR (p=0.9), MAP (p=0.22) and ETCO 2 (p=0.75) were similar across HOMA-IR. MAP (p=0.44) and ETCO 2 (p=0.15) did not change during OGTT at insulin peak. Peak insulin occurred at 44±13 min post OGTT (baseline: 8±4 vs. peak: 65±38 μU/mL, p=0.001). Glucose changed from 79±6 to 142±30 mg/dL at peak insulin (p=0.0005). There were no significant associations between HOMA-IR and changes in perfusion in gray matter (R 2 =0.06, p=0.43) and white matter (R 2 =0.07, p=0.13). There were no significant associations for the following regions: hippocampus, amygdala, thalamus, anterior and posterior insula, and precuneus (R 2 all <0.2, p all >0.14). There was a trend toward negative regression in anterior cingulate gyrus (R 2 =0.25, p=0.11). Conclusions: These data suggest an OGTT does not acutely change brain perfusion at a global or regional level in adolescents, except possibly the anterior cingulate gyrus that is negatively impacted by increasing IR. The majority of present findings do not support our hypothesis that OGTT-mediated changes in cerebral perfusion are associated with IR in adolescents. NIH R21HD097510 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Impact of increasing insulin resistance on cerebral perfusion in adolescents

Background: Adolescence is a key growth period that heavily influences future brain health. Approximately 1 in 5 adolescents are obese in the US, and up to half of them exhibit some form of insulin resistance (IR). Notably, insulin acts as a metabolic hormone, a neurotrophic growth factor, and a vasodilator. Reduced vasodilation may lead to reduced cerebral perfusion, and lower perfusion in older adults is associated with reduced cognition and increased risk of stroke and neurologic disease. Given this background, IR may negatively impact adolescent brain health in part due to lower brain perfusion. Therefore, we hypothesized cerebral perfusion would decrease as the level of insulin resistance increased. Method s: Adolescents (n=15, 4 females, age 15±2 yr) were studied. IR was estimated by calculating HOMA-IR (using fasting glucose and insulin), which spanned a spectrum of IR up to but excluding diabetes. Subjects underwent a magnetic resonance imaging (MRI) study visit to assess cerebral perfusion using arterial spin labeling (ASL). The CAT12 toolbox extension for SPM12 was used to process MRI data. Heart rate (HR), mean arterial pressure (MAP), and end tidal CO 2 (ETCO 2 ) were assessed. Significance was determined using linear regression and set at p≤0.05. Results: Results are mean±SD. HR (72±10 bpm, p=0.98), MAP (73±6 mmHg, p=0.67), and ETCO 2 (37±2 mmHg, p=0.91) were similar across HOMA-IR (0.5 to 3.8). Perfusion (ml/100g/min) at the amygdala (r 2 =0.33, p=0.02) and parahippocampal gyrus (r 2 =0.28, p=0.04) decreased as HOMA-IR increased. Borderline significant decreases were found for total gray matter (r 2 =0.26, p=0.051), anterior cingulate cortex (r 2 =0.26, p=0.052), and hippocampus (r 2 =0.23, p=0.07) perfusion as HOMA-IR increased. No associations were found between HOMA-IR and the following: total white matter (r 2 =0.18, p=0.11), precuneus (r 2 =0.20, p=0.10), thalamus proper (r 2 =0.14, p=0.17), and entorhinal cortex (r 2 =0.16, p=0.14) perfusion. Total gray matter (p=0.49) and white matter (p=0.73) volume had no significant relationship with HOMA-IR. HOMA-IR was not associated with any differences in regional volumes. Conclusions: Our results suggest with increasing HOMA-IR there is a significant reduction in gray matter perfusion in key brain regions associated with memory in adolescents. In contrast, structural changes were not detected, indicating functional decrements occur prior to structural deficits. These findings support our hypothesis that cerebral perfusion is associated with insulin resistance in adolescents, which may negatively impact long-term brain health. NIH R21 HD097510 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Indices of Inflammation, Oxidative Stress and DNA damage in T2DM patients with and without Insulin Therapy

Background: Type 2 Diabetes Mellitus is a metabolic disorder associated with excessive free radical generation and oxidative stress. Pharmacological interventions of T2DM targets on glycemic control and reduce the circulatory levels of oxidative stress and inflammation. Aim: The study compared the levels of oxidative stress, inflammation and the extent of DNA damage in T2DM patients undergoing different treatment modalities. Methods: 150 subjects recruited for this study belonged to the age group of 35-65 years. Participants were grouped as healthy controls (n=50), diabetics treated with oral hypoglycemic agent metformin (n=50) and diabetics undergoing combined therapy of insulin and metformin (n = 50). All the participants underwent the assessment of anthropometric measures, baseline blood pressure and blood samples were analysed for FBS, HbA1c, MDA, TAC, Hs-CRP and DNA damage. Results: Analysis using one-way ANOVA showed that despite the same age and duration of T2DM, patients in insulin therapy group had significantly higher levels of oxidative stress, inflammation and DNA damage when compared to T2DM patients treated with metformin alone. Further, significant correlations were observed for the above parameters with the duration of T2DM.Conclusion: The study concludes that oxidative stress, systemic inflammation and cellular senescence are more prominent in T2DM patients undergoing insulin therapy. Poor glycemic control observed in these patients could be attributed to increased insulin resistance as a consequence of oxidative stress and inflammation.

Insulin-like peptide 5 is associated with insulin resistance in women with polycystic ovary syndrome

AimsInsulin-like peptide 5 (INSL5) plays an important part in metabolic processes in vitro and in vivo. We hypothesized that INSL5 levels are associated with the presence of polycystic ovary syndrome (PCOS) and insulin resistance (IR). MethodsCirculating INSL5 levels were measured by an enzyme-linked immunosorbent assay in the PCOS group (n = 101) and control (n = 78) groups. The relationship between INSL5 and IR was evaluated by using regression models. ResultsThe levels of circulating INSL5 were elevated in the individuals with PCOS (P < 0.001) and significantly associated with homeostasis model assessment of insulin resistance (HOMA-IR, r = 0.434, P < 0.001; HOMA-IS, r = 0.432, P < 0.001; QUICKI, r = −0.504, P < 0.001). The subjects in the highest tertile of INSL5 levels were more likely to have PCOS (odds ratio: 12.591, 95 % confidence interval 2.616–60.605) as compared with the lowest tertile after adjustment for potential confounders. Furthermore, the multiple linear regression analyses after adjustment for confounders showed an independent association between INSL5 levels and HOMA-IR (β = 0.024, P < 0.001). ConclusionsCirculating INSL5 concentration is linked to PCOS, possibly through increased insulin resistance.

Does Insulin Resistance (IR) Have an Impact on The Reproductive and Fertility Potential in Polycystic Ovary Syndrome (PCOS) Women? : Review Article

Backgrounds: Polycystic ovary syndrome is the most common endocrine and reproductive disorder in the reproductive-age women. Among the pathological changes that are responsible for the development of polycystic ovary syndrome (PCOS), hyperinsulinemia due to increased insulin resistance (IR) is common and usually associated with a higher rate of ovulatory dysfunction and sub-fertility. In addition, those women have poor quality oocytes with low fertilization capability and poor quality embryos. So, insulin has a role in the reproductive function and fertility potential of reproductive age women. Conclusion: Females with PCOS usually exhibit an extreme difficulty in achieving either a successful spontaneous or assisted pregnancy. Hyperinsulinemia / insulin resistance and reproductive dysfunction should be well understood as can as possible in order to achieve an effective treatment plan to increase the chance of a successful uncomplicated pregnancy.

Reduced glucose tolerance and insulin sensitivity after prolonged exercise in endurance athletes.

The purpose of this study was to 1. investigate if glucose tolerance is affected after one acute bout of different types of exercise; 2. assess if potential differences between two exercise paradigms are related to changes in mitochondrial function; and 3. determine if endurance athletes differ from nonendurance-trained controls in their metabolic responses to the exercise paradigms. Nine endurance athletes (END) and eight healthy nonendurance-trained controls (CON) were studied. Oral glucose tolerance tests (OGTT) and mitochondrial function were assessed on three occasions: in the morning, 14 h after an overnight fast without prior exercise (RE), as well as after 3 h of prolonged continuous exercise at 65% of VO2 max (PE) or 5 × 4 min at ~95% of VO2 max (HIIT) on a cycle ergometer. Glucose tolerance was markedly reduced in END after PE compared with RE. END also exhibited elevated fasting serum FFA and ketones levels, reduced insulin sensitivity and glucose oxidation, and increased fat oxidation during the OGTT. CON showed insignificant changes in glucose tolerance and the aforementioned measurements compared with RE. HIIT did not alter glucose tolerance in either group. Neither PE nor HIIT affected mitochondrial function in either group. END also exhibited increased activity of 3-hydroxyacyl-CoA dehydrogenase activity in muscle extracts vs. CON. Prolonged exercise reduces glucose tolerance and increases insulin resistance in endurance athletes the following day. These findings are associated with an increased lipid load, a high capacity to oxidize lipids, and increased fat oxidation.

Dynamic Changes of BVRA Protein Levels Occur in Response to Insulin: A Pilot Study in Humans.

Biliverdin reductase-A (BVRA) is involved in the regulation of insulin signaling and the maintenance of glucose homeostasis. Previous research showed that BVRA alterations are associated with the aberrant activation of insulin signaling in dysmetabolic conditions. However, whether BVRA protein levels change dynamically within the cells in response to insulin and/or glucose remains an open question. To this aim, we evaluated changes of intracellular BVRA levels in peripheral blood mononuclear cells (PBMC) collected during the oral glucose tolerance test (OGTT) in a group of subjects with different levels of insulin sensitivity. Furthermore, we looked for significant correlations with clinical measures. Our data show that BVRA levels change dynamically during the OGTT in response to insulin, and greater BVRA variations occur in those subjects with lower insulin sensitivity. Changes of BVRA significantly correlate with indexes of increased insulin resistance and insulin secretion (HOMA-IR, HOMA-β, and insulinogenic index). At the multivariate regression analysis, the insulinogenic index independently predicted increased BVRA area under curve (AUC) during the OGTT. This pilot study showed, for the first time, that intracellular BVRA protein levels change in response to insulin during OGTT and are greater in subjects with lower insulin sensitivity, supporting the role of BVR-A in the dynamic regulation of the insulin signaling pathway.

Association of preterm birth with poor metabolic outcomes in schoolchildren

ObjectiveTo investigate, at school age, the metabolic profile of children born preterm. MethodsA cross-sectional study of children 5 to 8 years old, born with gestational age (GA) < 34 weeks and/or weight ≤ 1,500 grams. Clinical and anthropometric data were assessed by a single trained pediatrician. Biochemical measurements were done at the organization's Central Laboratory using standard methods. Data on health conditions, eating, and daily life habits were retrieved from medical charts and through validated questionnaires. Binary logistic and linear regression models were built to identify the association between variables, weight excess, and GA. ResultsOut of 60 children (53.3% female), 6.8 ± 0.7 years old, 16.6% presented excess weight, 13.3% showed increased insulin resistance markers and 36.7% had abnormal blood pressure values. Those presenting excess weight had higher waist circumferences and higher HOMA-IR than normal-weight children (OR = 1.64; CI = 1.035–2.949). Eating and daily life habits were not different among overweight and normal-weight children. The small-for-gestational-age (SGA) and appropriate-for-gestational-age (AGA, 83.3%) birth weight children did not differ regarding clinical (body weight, blood pressure) or biochemical variables (serum lipids, blood glucose, HOMA-IR). ConclusionSchoolchildren born preterm, regardless of being AGA or SGA, were overweight, and presented increased abdominal adiposity, reduced insulin sensitivity, and altered lipid profile, justifying longitudinal follow-up regarding adverse metabolic outcomes in the future.

MP45-07 ERECTILE DYSFUNCTION AND HYPOGONADISM ARE UNDERREPORTED IN MEN WITH SPINA BIFIDA

You have accessJournal of UrologyCME1 Apr 2023MP45-07 ERECTILE DYSFUNCTION AND HYPOGONADISM ARE UNDERREPORTED IN MEN WITH SPINA BIFIDA Nyemkuna Fortingo, Garrick Greear, Tung-Chin Hsieh, Rupam Das, Joshua Horns, James Hotaling, and Yahir Santiago-Lastra Nyemkuna FortingoNyemkuna Fortingo More articles by this author , Garrick GreearGarrick Greear More articles by this author , Tung-Chin HsiehTung-Chin Hsieh More articles by this author , Rupam DasRupam Das More articles by this author , Joshua HornsJoshua Horns More articles by this author , James HotalingJames Hotaling More articles by this author , and Yahir Santiago-LastraYahir Santiago-Lastra More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000003291.07AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Spina Bifida is a congenital neurological defect associated with genitourinary anomalies, requiring comprehensive urological care from pediatrics to adulthood. For men with spina bifida, a significant focus is on urinary tract surveillance to maintain continence, preserve kidney and bladder health, and optimize fertility and sexual function. While men with SB have an increasing interest in exploring their sexuality and sexual health, these concerns may be under-discussed and undertreated depending on their burden of illness. Concurrently, the impact of hypogonadism on the SB is unknown. Hypogonadism is associated with increased insulin resistance in young males, hyperlipidemia, and other adverse vascular effects. These risk factors play a role in the vascular etiology of erectile dysfunction and can be a burden on sexual health. Our objective was to calculate the estimated prevalence of erectile dysfunction and hypogonadism in adult men with spina bifida. METHODS: This retrospective claims study used the MarketScan® databases from 2008 to 2017 to derive prevalence estimates for erectile dysfunction and hypogonadism in men with spina bifida, to compare these estimates to those in men without spina bifida, and to describe treatment patterns in this cohort. RESULTS: The estimated prevalence of erectile dysfunction and hypogonadism in men with spina bifida was 7.83% and 7.71%, respectively. Men with spina bifida in the sample exhibited high rates of smoking and metabolic comorbidities, but were diagnosed less frequently with erectile dysfunction when controlling for age and metabolic comorbidities than men without spina bifida. CONCLUSIONS: Based on the results, claims data suggest that HG and ED are diagnosed less frequently than expected. While there are some limitations to the population being examined in this database, improving health care delivery of sexual health concerns during the surveillance of men with spina bifida will enhance their quality of life and optimize their sexual and metabolic function. Source of Funding: N/A © 2023 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 209Issue Supplement 4April 2023Page: e623 Advertisement Copyright & Permissions© 2023 by American Urological Association Education and Research, Inc.MetricsAuthor Information Nyemkuna Fortingo More articles by this author Garrick Greear More articles by this author Tung-Chin Hsieh More articles by this author Rupam Das More articles by this author Joshua Horns More articles by this author James Hotaling More articles by this author Yahir Santiago-Lastra More articles by this author Expand All Advertisement PDF downloadLoading ...

NAFLD: A pretransplant and post-transplant conundrum.

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PD21-08 PERSISTENT TESTOSTERONE SUPPRESSION AFTER CESSATION OF ANDROGEN DEPRIVATION THERAPY FOR PROSTATE CANCER

You have accessJournal of UrologyCME1 Apr 2023PD21-08 PERSISTENT TESTOSTERONE SUPPRESSION AFTER CESSATION OF ANDROGEN DEPRIVATION THERAPY FOR PROSTATE CANCER Nicholas Deebel, Jessica Delgado, Jesse Ory, Justin Loloi, Ari Bernstein, Sirpi Nackeeran, and Ranjith Ramasamy Nicholas DeebelNicholas Deebel More articles by this author , Jessica DelgadoJessica Delgado More articles by this author , Jesse OryJesse Ory More articles by this author , Justin LoloiJustin Loloi More articles by this author , Ari BernsteinAri Bernstein More articles by this author , Sirpi NackeeranSirpi Nackeeran More articles by this author , and Ranjith RamasamyRanjith Ramasamy More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000003287.08AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Androgen deprivation therapy (ADT) is frequently used in the treatment of localized PCa. Many men receiving temporary ADT for localized prostate cancer fail to achieve baseline testosterone (T) levels after cessation. However, current literature limits the ability to predict prolonged testosterone deficiency (TD) based on ADT regimen and duration. Testosterone recovery in men with localized prostate cancer receiving temporary ADT was assessed. METHODS: A globally federated health research network (TriNetX) was used to identify men diagnosed with prostate cancer undergoing temporary ADT. Inclusion criteria consisted of: a clinically localized prostate cancer and eugonadal mean baseline T level (>300 ng/dL). Prior to starting ADT two cohorts were identified: Men receiving LHRH antagonists or LHRH agonists and men receiving combined ADT (LHRH agonist and antiandrogens). Further stratification was based on treatment duration of 6 months (short-term) or 18 months (long-term) to compare T recovery profiles 5 years after ADT cessation. RESULTS: A total of 28,583 men received LHRH agonist or antagonist therapy alone and 20,188 men received combination ADT. A total of 46.7% of men who received short-term LHRH agonists or antagonists and 40.6% of men who received short-term combined ADT recovered to mean baseline T levels at 5 years (p = 0.06). Only men who received short-term LHRH agonist/antagonists recovered to a mean eugonadal level at 5 year follow-up. Meanwhile, 50% of men who received long-term LHRH agonist/antagonist therapy and 10.7% of men who received long-term combined ADT recovered to mean baseline T levels at 5 years (p < 0.0001). However, neither group recovered to a mean eugonadal T level. CONCLUSIONS: Most patients failed to recover to mean baseline and eugonadal T levels at 5-year follow-up. Given that TD is associated with a myriad of adverse effects such as metabolically adverse changes in body composition, increased insulin resistance, impaired bone health, and hypogonadal symptoms, serum T levels must be closely followed in men receiving ADT following treatment cessation. Source of Funding: NIH Grant R01 DK130991 and Clinician Scientist Development Grant from the ACS to RR © 2023 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 209Issue Supplement 4April 2023Page: e593 Advertisement Copyright & Permissions© 2023 by American Urological Association Education and Research, Inc.MetricsAuthor Information Nicholas Deebel More articles by this author Jessica Delgado More articles by this author Jesse Ory More articles by this author Justin Loloi More articles by this author Ari Bernstein More articles by this author Sirpi Nackeeran More articles by this author Ranjith Ramasamy More articles by this author Expand All Advertisement PDF downloadLoading ...

A STUDY OF CORRELATION BETWEEN GAMMA GLUTAMYL TRANSFERASE AND METABOLIC SYNDROME

CONTEXT:The metabolic syndrome ( Syndrome X, or insulin resistance syndrome) is a combination of several risk factors that contribute to atherosclerotic cardiovascular disease (ASCVD). Elevated blood pressure, triglycerides, hyperglycemia, waist circumference and low HDL- cholesterol are all symptoms of accelerated dyslipidemic atherogenesis. Glutamyl transferase (GGT) has long been thought to be a biomarker for hepatic and biliary illness and alcoholic related disease. GGT is required for the extracellular catabolism of glutathione, which is the most important thiol antioxidant in humans.It co localizes with oxidised low density lipoprotein (LDL) and foam cells in the atheromatous core of coronary plaques. GGT can be a proinammatory sign. GGT was found to be a prognostic marker for Metabolic syndrome, CVD, and heart failure .AIM: Study of Gamma glutamyltransferase in metabolic syndrome patients. MATERIALS AD METHODS: A sample size of 100 patients admitted in medicine and other departments in nri general hospital are included in study Qualitative data was expressed in frequencies and percentages a STASTISTICAL ANALYSIS: nd Quantitative data in mean and standard deviation. Non parametric statistics i.e. Chisquare test was used to nd the signicant association between the two qualitative variables. Independent t test and ANOVA were used to nd the statistical signicance between quantitative variables. Pearson correlation coefcient was used to nd correlation between two variables. p value of &lt;0.05was considered statistically signicant. CONCLUSION: It should be highlighted that elevated levels of GGT are not the only hepatic biomarker of hepatic steatosis, as evidenced by ndings from several research. lines of evidence point to a link between high GGT levels in the blood and the metabolic syndrome. As a result, higher GGT levels are associated with increased insulin resistance and a higher risk of type 2 diabetes .

Effect of High Fat and Cholesterol Diet on Total Blood Cholesterol Levels in Pregnant Wistar Rats

Hypercholesterolemia during pregnancy is a physiological condition resulting from increased insulin resistance, lipoprotein synthesis, and lipolysis in adipose tissue, which mobilizes lipids as an energetic substrate for fetal growth. Consumption of foods high in fat and cholesterol may lead to an increase in total blood cholesterol levels during pregnancy due to saturated fat and cholesterol contents that will increases the synthesis of lipoproteins in the blood. The objectives of this study were to determine the effects of high fat and cholesterol diet on the total blood cholesterol levels in pregnant Wistar rats. This study was a true experimental research using a randomized post-test-only control group design conducted from November 2020 to October 2021on fourteen female Wistar rats that were divided into control and intervention groups. Cow brain was provided as the high fat and cholesterol diet and after the rats gave birth, blood was drawn from the heart. The total blood serum cholesterol levels were assessed using Micro Lab 300 with the CHOD-PAP method and the data were analyzed using an independent t-test. This study showed that the mean total blood cholesterol levels for the control and treatment groups were 80.43±18.512 mg/dL and 142.57±24.786 mg/dL, respectively, which reflected a significant differences in the mean total blood cholesterol level between the control and treatment groups (p-value &lt;0.01). In conclusion, a high fat and cholesterol diet affects the total blood cholesterol level in pregnant Wistar rats.

Elevated Maternal Folate Status and Changes in Maternal Prolactin, Placental Lactogen and Placental Growth Hormone Following Folic Acid Food Fortification: Evidence from Two Prospective Pregnancy Cohorts.

Folic acid (FA) food fortification in Australia has resulted in a higher-than-expected intake of FA during pregnancy. High FA intake is associated with increased insulin resistance and gestational diabetes. We aimed to establish whether maternal one-carbon metabolism and hormones that regulate glucose homeostasis change in healthy pregnancies post-FA food fortification. Circulating folate, B12, homocysteine, prolactin (PRL), human placental lactogen (hPL) and placental growth hormone (GH2) were measured in early pregnancy maternal blood in women with uncomplicated pregnancies prior to (SCOPE: N = 604) and post (STOP: N = 711)-FA food fortification. FA food fortification resulted in 63% higher maternal folate. STOP women had lower hPL (33%) and GH2 (43%) after 10 weeks of gestation, but they had higher PRL (29%) and hPL (28%) after 16 weeks. FA supplementation during pregnancy increased maternal folate and reduced homocysteine but only in the SCOPE group, and it was associated with 54% higher PRL in SCOPE but 28% lower PRL in STOP. FA food fortification increased maternal folate status, but supplements no longer had an effect, thereby calling into question their utility. An altered secretion of hormones that regulate glucose homeostasis in pregnancy could place women post-fortification at an increased risk of insulin resistance and gestational diabetes, particularly for older women and those with obesity.