Search Results
Search for other papers by Ghazala Zaidi in
Google Scholar
PubMed
Search for other papers by Vijayalakshmi Bhatia in
Google Scholar
PubMed
Search for other papers by Saroj K Sahoo in
Google Scholar
PubMed
Search for other papers by Aditya Narayan Sarangi in
Google Scholar
PubMed
Search for other papers by Niharika Bharti in
Google Scholar
PubMed
Search for other papers by Li Zhang in
Google Scholar
PubMed
Search for other papers by Liping Yu in
Google Scholar
PubMed
Search for other papers by Daniel Eriksson in
Google Scholar
PubMed
Search for other papers by Sophie Bensing in
Google Scholar
PubMed
Science for Life Laboratory, Department of Medical Sciences, Uppsala University, Sweden
Search for other papers by Olle Kämpe in
Google Scholar
PubMed
Search for other papers by Nisha Bharani in
Google Scholar
PubMed
Search for other papers by Surendra Kumar Yachha in
Google Scholar
PubMed
Search for other papers by Anil Bhansali in
Google Scholar
PubMed
Search for other papers by Alok Sachan in
Google Scholar
PubMed
Search for other papers by Vandana Jain in
Google Scholar
PubMed
Search for other papers by Nalini Shah in
Google Scholar
PubMed
Search for other papers by Rakesh Aggarwal in
Google Scholar
PubMed
Search for other papers by Amita Aggarwal in
Google Scholar
PubMed
Search for other papers by Muthuswamy Srinivasan in
Google Scholar
PubMed
Search for other papers by Sarita Agarwal in
Google Scholar
PubMed
Search for other papers by Eesh Bhatia in
Google Scholar
PubMed
Objective
Autoimmune polyendocrine syndrome type 1 (APS1) is a rare autosomal recessive disorder characterized by progressive organ-specific autoimmunity. There is scant information on APS1 in ethnic groups other than European Caucasians. We studied clinical aspects and autoimmune regulator (AIRE) gene mutations in a cohort of Indian APS1 patients.
Design
Twenty-three patients (19 families) from six referral centres in India, diagnosed between 1996 and 2016, were followed for [median (range)] 4 (0.2–19) years.
Methods
Clinical features, mortality, organ-specific autoantibodies and AIRE gene mutations were studied.
Results
Patients varied widely in their age of presentation [3.5 (0.1–17) years] and number of clinical manifestations [5 (2–11)]. Despite genetic heterogeneity, the frequencies of the major APS1 components (mucocutaneous candidiasis: 96%; hypoparathyroidism: 91%; primary adrenal insufficiency: 55%) were similar to reports in European series. In contrast, primary hypothyroidism (23%) occurred more frequently and at an early age, while kerato-conjunctivitis, urticarial rash and autoimmune hepatitis were uncommon (9% each). Six (26%) patients died at a young age [5.8 (3–23) years] due to septicaemia, hepatic failure and adrenal/hypocalcaemic crisis from non-compliance/unexplained cause. Interferon-α and/or interleukin-22 antibodies were elevated in all 19 patients tested, including an asymptomatic infant. Eleven AIRE mutations were detected, the most common being p.C322fsX372 (haplotype frequency 37%). Four mutations were novel, while six others were previously described in European Caucasians.
Conclusions
Indian APS1 patients exhibited considerable genetic heterogeneity and had highly variable clinical features. While the frequency of major manifestations was similar to that of European Caucasians, other features showed significant differences. A high mortality at a young age was observed.
Search for other papers by Lia Ferreira in
Google Scholar
PubMed
Search for other papers by João Silva in
Google Scholar
PubMed
Search for other papers by Susana Garrido in
Google Scholar
PubMed
Search for other papers by Carlos Bello in
Google Scholar
PubMed
Search for other papers by Diana Oliveira in
Google Scholar
PubMed
Search for other papers by Hélder Simões in
Google Scholar
PubMed
Search for other papers by Isabel Paiva in
Google Scholar
PubMed
Search for other papers by Joana Guimarães in
Google Scholar
PubMed
Search for other papers by Marta Ferreira in
Google Scholar
PubMed
Search for other papers by Teresa Pereira in
Google Scholar
PubMed
Search for other papers by Rita Bettencourt-Silva in
Google Scholar
PubMed
Search for other papers by Ana Filipa Martins in
Google Scholar
PubMed
Search for other papers by Tiago Silva in
Google Scholar
PubMed
Search for other papers by Vera Fernandes in
Google Scholar
PubMed
Search for other papers by Maria Lopes Pereira in
Google Scholar
PubMed
Search for other papers by Adrenal Tumors Study Group of the Portuguese Society of Endocrinology in
Google Scholar
PubMed
Introduction
Primary adrenal insufficiency (PAI) is a rare but severe and potentially life-threatening condition. No previous studies have characterized Portuguese patients with PAI.
Aims
To characterize the clinical presentation, diagnostic workup, treatment and follow‐up of Portuguese patients with confirmed PAI.
Methods
This multicentre retrospective study examined PAI patients in 12 Portuguese hospitals.
Results
We investigated 278 patients with PAI (55.8% were females), with a mean age of 33.6 ± 19.3 years at diagnosis. The most frequent presenting clinical features were asthenia (60.1%), mucocutaneous hyperpigmentation (55.0%) and weight loss (43.2%); 29.1% of the patients presented with adrenal crisis. Diagnosis was established by high plasma ACTH and low serum cortisol in most patients (43.9%). The most common aetiology of PAI was autoimmune adrenalitis (61.0%). There were 38 idiopathic cases. Autoimmune comorbidities were found in 70% of the patients, the most frequent being autoimmune thyroiditis (60.7%) and type 1 diabetes mellitus (17.3%). Seventy-nine percent were treated with hydrocortisone (mean dose 26.3 ± 8.3 mg/day) mostly in three (57.5%) or two (37.4%) daily doses. The remaining patients were treated with prednisolone (10.1%), dexamethasone (6.2%) and methylprednisolone (0.7%); 66.2% were also on fludrocortisone (median dose of 100 µg/day). Since diagnosis, 33.5% of patients were hospitalized for disease decompensation. In the last appointment, 17.2% of patients had complaints (7.6% asthenia and 6.5% depression) and 9.7% had electrolyte disturbances.
Conclusion
This is the first multicentre Portuguese study regarding PAI. The results emphasize the need for standardization in diagnostic tests and etiological investigation and provide a framework for improving treatment.
K.G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Search for other papers by Elinor Chelsom Vogt in
Google Scholar
PubMed
Department of Gynecology and Obstetrics, Haukeland University Hospital, Bergen, Norway
Search for other papers by Francisco Gómez Real in
Google Scholar
PubMed
K.G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Search for other papers by Eystein Sverre Husebye in
Google Scholar
PubMed
Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden
Search for other papers by Sigridur Björnsdottir in
Google Scholar
PubMed
Department of Sleep, Landspitali University Hospital Reykjavík, Reykjavik, Iceland
Search for other papers by Bryndis Benediktsdottir in
Google Scholar
PubMed
Search for other papers by Randi Jacobsen Bertelsen in
Google Scholar
PubMed
Search for other papers by Pascal Demoly in
Google Scholar
PubMed
Search for other papers by Karl Anders Franklin in
Google Scholar
PubMed
Search for other papers by Leire Sainz de Aja Gallastegui in
Google Scholar
PubMed
Search for other papers by Francisco Javier Callejas González in
Google Scholar
PubMed
Allergy and Lung Health Unit, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Victoria, Australia
Search for other papers by Joachim Heinrich in
Google Scholar
PubMed
Search for other papers by Mathias Holm in
Google Scholar
PubMed
Search for other papers by Nils Oscar Jogi in
Google Scholar
PubMed
Search for other papers by Benedicte Leynaert in
Google Scholar
PubMed
Search for other papers by Eva Lindberg in
Google Scholar
PubMed
Search for other papers by Andrei Malinovschi in
Google Scholar
PubMed
Albacete Faculty of Medicine, Castilla-La Mancha University, Albacete, Spain
Search for other papers by Jesús Martínez-Moratalla in
Google Scholar
PubMed
Search for other papers by Raúl Godoy Mayoral in
Google Scholar
PubMed
Search for other papers by Anna Oudin in
Google Scholar
PubMed
Search for other papers by Antonio Pereira-Vega in
Google Scholar
PubMed
Search for other papers by Chantal Raherison Semjen in
Google Scholar
PubMed
The National Research Center for the Working Environment, Copenhagen, Denmark
Search for other papers by Vivi Schlünssen in
Google Scholar
PubMed
Search for other papers by Kai Triebner in
Google Scholar
PubMed
K.G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Search for other papers by Marianne Øksnes in
Google Scholar
PubMed
Objective
To investigate markers of premature menopause (<40 years) and specifically the prevalence of autoimmune primary ovarian insufficiency (POI) in European women.
Design
Postmenopausal women were categorized according to age at menopause and self-reported reason for menopause in a cross-sectional analysis of 6870 women.
Methods
Variables associated with the timing of menopause and hormone measurements of 17β-estradiol and follicle-stimulating hormone were explored using multivariable logistic regression analysis. Specific immunoprecipitating assays of steroidogenic autoantibodies against 21-hydroxylase (21-OH), side-chain cleavage enzyme (anti-SCC) and 17alpha-hydroxylase (17 OH), as well as NACHT leucine-rich-repeat protein 5 were used to identify women with likely autoimmune POI.
Results
Premature menopause was identified in 2.8% of women, and these women had higher frequencies of nulliparity (37.4% vs 19.7%), obesity (28.7% vs 21.4%), osteoporosis (17.1% vs 11.6%), hormone replacement therapy (59.1% vs 36.9%) and never smokers (60.1% vs 50.9%) (P < 0.05), compared to women with menopause ≥40 years. Iatrogenic causes were found in 91 (47%) and non-ovarian causes in 27 (14%) women, while 77 (39%) women were classified as POI of unknown cause, resulting in a 1.1% prevalence of idiopathic POI. After adjustments nulliparity was the only variable significantly associated with POI (odds ratio 2.46; 95% CI 1.63–3.42). Based on the presence of autoantibodies against 21 OH and SCC, 4.5% of POI cases were of likely autoimmune origin.
Conclusion
Idiopathic POI affects 1.1% of all women and almost half of the women with premature menopause. Autoimmunity explains 4.5% of these cases judged by positive steroidogenic autoantibodies.
Search for other papers by Sriharsha Gunna in
Google Scholar
PubMed
Search for other papers by Mahaveer Singh in
Google Scholar
PubMed
Search for other papers by Rakesh Pandey in
Google Scholar
PubMed
Search for other papers by Rungmei S K Marak in
Google Scholar
PubMed
Search for other papers by Amita Aggarwal in
Google Scholar
PubMed
Search for other papers by Bibhuti Mohanta in
Google Scholar
PubMed
Search for other papers by Liping Yu in
Google Scholar
PubMed
Search for other papers by Eesh Bhatia in
Google Scholar
PubMed
The etiology, presentation and mortality of patients with primary adrenal insufficiency (PAI) in developing countries may differ from economically developed nations. However, information in this regard is scanty. The aim of this study was to determine the etiology and compare the clinical characteristics and mortality in infectious and autoimmune causes of PAI in Indian patients. All eligible (n = 89) patients (ages 15–83 years) diagnosed with PAI between 2006 and 2019 were studied. Patients were followed for a median duration of 5.9 (range 0.1–15.7) years. Eighty-six subjects underwent an abdominal computerized tomography scan or ultrasonography, and adrenal biopsy was performed in 60 patients. The most frequent etiologies of PAI were adrenal histoplasmosis (AH, 45%), adrenal tuberculosis (AT, 15%), autoimmunity (AI, 25%) and primary lymphoma (6%). Forty-two percent of patients presented with an acute adrenal crisis. AH and AT could not be differentiated on the basis of clinical features, except for a greater frequency of hepatomegaly–splenomegaly and type 2 diabetes mellitus (63% vs 15%, P < 0.01) in the former. Patients with an autoimmune etiology had a higher frequency of 21-hydroxylase antibodies (41% vs 3%) and autoimmune thyroid disease (46% vs 5%) vs those with infectious etiologies. Mortality was significantly higher in AH (45%) compared with AT (8%) or AI (5%) (P = 0.001). Causes of death included adrenal crises, progressive AH and unexplained acute events occurring at home. In conclusion, infections, especially AH, were the most frequent cause of PAI in north India. Despite appropriate therapy, AH had very high mortality as compared with AT and AI.
The Leicester Diabetes Centre, University Hospitals of Leicester NHS Trust, Leicester General Hospital, Leicester, UK
Search for other papers by M A Webb in
Google Scholar
PubMed
Department of Diabetes and Endocrinology, Leicester Royal Infirmary, University Hospitals of Leicester NHS Trust, Leicester, UK
Diabetes and Endocrinology Department, Kettering General Hospital NHS Foundation Trust, Kettering, UK
Search for other papers by H Mani in
Google Scholar
PubMed
Search for other papers by S J Robertson in
Google Scholar
PubMed
Search for other papers by H L Waller in
Google Scholar
PubMed
Diabetes Research Centre, University of Leicester, Leicester General Hospital, Leicester, UK
Search for other papers by D R Webb in
Google Scholar
PubMed
Diabetes Research Centre, University of Leicester, Leicester General Hospital, Leicester, UK
Search for other papers by C L Edwardson in
Google Scholar
PubMed
Diabetes Research Centre, University of Leicester, Leicester General Hospital, Leicester, UK
Search for other papers by D H Bodicoat in
Google Scholar
PubMed
Diabetes Research Centre, University of Leicester, Leicester General Hospital, Leicester, UK
Search for other papers by T Yates in
Google Scholar
PubMed
The Leicester Diabetes Centre, University Hospitals of Leicester NHS Trust, Leicester General Hospital, Leicester, UK
Diabetes Research Centre, University of Leicester, Leicester General Hospital, Leicester, UK
Search for other papers by K Khunti in
Google Scholar
PubMed
The Leicester Diabetes Centre, University Hospitals of Leicester NHS Trust, Leicester General Hospital, Leicester, UK
Diabetes Research Centre, University of Leicester, Leicester General Hospital, Leicester, UK
Search for other papers by M J Davies in
Google Scholar
PubMed
Aims
Physical activity has been proposed to be an effective non-pharmacological method of reducing systemic inflammation and therefore may prove particularly efficacious for women with polycystic ovary syndrome (PCOS) who have been shown to have high levels of inflammation and an increased risk of type 2 diabetes (T2DM) and cardiovascular disease (CVD). Therefore, the aim of the present study was to assess whether modest changes in daily step count could significantly reduce levels of inflammatory markers in women with PCOS.
Subjects and Methods
Sixty-five women with PCOS were assessed at baseline and again at 6 months. All had been provided with an accelerometer and encouraged to increase activity levels. Multivariate linear regression analyses (adjusted for age, ethnicity, baseline step count, change in BMI and change in accelerometer wear-time) were used to assess changes in daily step count against clinical and research biomarkers of inflammation, CVD and T2DM.
Results
Mean step count/day at baseline was 6337 (±270). An increase in step count (by 1000 steps) was associated with a 13% reduction in IL6 (β: −0.81 ng/L; 95% CI, −1.37, −0.25, P = 0.005) and a 13% reduction in CRP (β: −0.68 mg/L; 95% CI, −1.30, −0.06, P = 0.033). Additionally, there was a modest decrease in BMI (β: 0.20 kg/m2; 95% CI, −0.38, −0.01, P = 0.038). Clinical markers of T2DM and CVD were not affected by increased step count.
Conclusions
Modest increases in step count/day can reduce levels of inflammatory markers in women with PCOS, which may reduce the future risk of T2DM and CVD.
Department of Clinical Research, University of Basel and University Hospital Basel, Basel, Switzerland
Search for other papers by Milica Popovic in
Google Scholar
PubMed
Department of Clinical Research, University of Basel and University Hospital Basel, Basel, Switzerland
Search for other papers by Fahim Ebrahimi in
Google Scholar
PubMed
Department of Clinical Research, University of Basel and University Hospital Basel, Basel, Switzerland
Search for other papers by Sandrine Andrea Urwyler in
Google Scholar
PubMed
Department of Biomedicine, University of Basel, Basel, Switzerland
Search for other papers by Marc Yves Donath in
Google Scholar
PubMed
Department of Clinical Research, University of Basel and University Hospital Basel, Basel, Switzerland
Search for other papers by Mirjam Christ-Crain in
Google Scholar
PubMed
Arginine vasopressin (AVP) was suggested to contribute to cardiovascular risk and type 2 diabetes in patients with metabolic syndrome. The proinflammatory cytokine interleukin (IL)-1 is able to induce AVP secretion and plays a causal role in cardiovascular mortality and type 2 diabetes. We investigated in two studies whether copeptin levels – the surrogate marker for AVP – are regulated by IL-1-mediated chronic inflammation in patients with metabolic syndrome. Study A was a prospective, interventional, single-arm study (2014–2016). Study B was a randomized, placebo-controlled, double-blind study (2016–2017). n = 73 (Study A) and n = 66 (Study B) adult patients with metabolic syndrome were treated with 100 mg anakinra or placebo (only in study B) twice daily for 1 day (study A) and 28 days (study B). Fasting blood samples were drawn at day 1, 7, and 28 of treatment for measurement of serum copeptin. Patients with chronic low-grade inflammation (C-reactive protein levels ≥2 mg/L) and BMI >35 kg/m2 had higher baseline copeptin levels (7.7 (IQR 4.9–11.9) vs 5.8 (IQR 3.9–9.3) pmol/L, P inflamm = 0.009; 7.8 (IQR 5.4–11.7) vs 4.9 (IQR 3.7–9.8) pmol/L, P BMI = 0.008). Copeptin levels did not change either in the anakinra or in the placebo group and remained stable throughout the treatment (P = 0.44). Subgroup analyses did not reveal effect modifications. Therefore, we conclude that, although IL-1-mediated inflammation is associated with increased circulating copeptin levels, antagonizing IL-1 does not significantly alter copeptin levels in patients with metabolic syndrome.
Search for other papers by Xiao-Shan Huang in
Google Scholar
PubMed
Search for other papers by Ning Dai in
Google Scholar
PubMed
Search for other papers by Jian-Xia Xu in
Google Scholar
PubMed
Search for other papers by Jun-Yi Xiang in
Google Scholar
PubMed
Search for other papers by Xiao-Zhong Zheng in
Google Scholar
PubMed
Search for other papers by Tian-Yu Ke in
Google Scholar
PubMed
Search for other papers by Lin-Ying Ma in
Google Scholar
PubMed
Search for other papers by Qi-Hao Shi in
Google Scholar
PubMed
Search for other papers by Shu-Feng Fan in
Google Scholar
PubMed
Objective
Hashimoto’s thyroiditis is an inflammatory disease, and research suggests that a low-carbohydrate diet may have potential anti-inflammatory effects. This study aims to utilize Dixon-T2-weighted imaging (WI) sequence for a semi-quantitative assessment of the impact of a low-carbohydrate diet on the degree of thyroid inflammation in patients with Hashimoto’s thyroiditis.
Methods
Forty patients with Hashimoto’s thyroiditis were recruited for this study and randomly divided into two groups: one with a normal diet and the other with a low-carbohydrate diet. Antibodies against thyroid peroxidase (TPOAb) and thyroglobulin (TgAb) were measured for all participants. Additionally, thyroid water content was semi-quantitatively measured using Dixon-T2WI. The same tests and measurements were repeated for all participants after 6 months.
Results
After 6 months of a low-carbohydrate diet, patients with Hashimoto’s thyroiditis showed a significant reduction in thyroid water content (94.84 ± 1.57% vs 93.07 ± 2.05%, P < 0.05). Concurrently, a decrease was observed in levels of TPOAb and TgAb (TPOAb: 211.30 (92.63–614.62) vs 89.45 (15.9–215.67); TgAb: 17.05 (1.47–81.64) vs 4.1 (0.51–19.42), P < 0.05). In contrast, there were no significant differences in thyroid water content or TPOAb and TgAb levels for patients with Hashimoto’s thyroiditis following a normal diet after 6 months (P < 0.05).
Conclusion
Dixon-T2WI can quantitatively assess the degree of thyroid inflammation in patients with Hashimoto’s thyroiditis. Following a low-carbohydrate diet intervention, there is a significant reduction in thyroid water content and a decrease in levels of TPOAb and TgAb. These results suggest that a low-carbohydrate diet may help alleviate inflammation in patients with Hashimoto’s thyroiditis.
Search for other papers by Borros Arneth in
Google Scholar
PubMed
Background
The origin of autoimmune disease type 1 diabetes is still unknown.
Aim
This study assessed the activation of CD4+ and CD8+ T-lymphocytes by human insulin and human glutamate decarboxylase (GAD) in patients with type 1 or type 2 diabetes mellitus (DM) and healthy volunteers.
Materials and methods
The expression of CD69, a marker of T-lymphocyte activity, was determined in whole blood samples by flow cytometry after 12 h of incubation with or without insulin or GAD. The analysis included samples from 12 type 1 DM patients, 14 type 2 DM patients and 12 healthy volunteers.
Results
Significant increases in the number of activated CD4+ and CD8+ T-lymphocytes following pre-incubation of whole blood samples with human insulin or GAD were observed in samples from patients with type 1 DM, whereas no activation of these cells was detected in samples from either type 2 DM patients or healthy subjects.
Discussion
These results indicated that latent pre-activation of CD4+ and CD8+ T-lymphocytes in response to insulin or GAD epitopes occurred in type 1 DM patients.
Conclusion
These findings suggest that pre-immunization against insulin and/or GAD might be associated with the development of type 1 DM. Alternatively, these results might reflect a non-specific, bystander autoimmune response.
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China
Search for other papers by Liangming Li in
Google Scholar
PubMed
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China
Search for other papers by Yuan Wei in
Google Scholar
PubMed
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China
Search for other papers by Chunlu Fang in
Google Scholar
PubMed
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China
Search for other papers by Shujing Liu in
Google Scholar
PubMed
Search for other papers by Fu Zhou in
Google Scholar
PubMed
Search for other papers by Ge Zhao in
Google Scholar
PubMed
Search for other papers by Yaping Li in
Google Scholar
PubMed
Search for other papers by Yuan Luo in
Google Scholar
PubMed
Search for other papers by Ziyi Guo in
Google Scholar
PubMed
Search for other papers by Weiqun Lin in
Google Scholar
PubMed
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China
Search for other papers by Wenqi Yang in
Google Scholar
PubMed
Exercise has been recommended as an important strategy to improve glucose metabolism in obesity. Adipose tissue fibrosis is associated with inflammation and is implicated in glucose metabolism disturbance and insulin resistance in obesity. However, the effect of exercise on the progression of adipose tissue fibrosis is still unknown. The aim of the present study was to investigate whether exercise retarded the progression of adipose tissue fibrosis and ameliorated glucose homeostasis in diet-induced obese mice. To do so, obesity and adipose tissue fibrosis in mice were induced by high-fat diet feeding for 12 weeks and the mice subsequently received high-fat diet and exercise intervention for another 12 weeks. Exercise alleviated high-fat diet-induced glucose intolerance and insulin resistance. Continued high-fat diet feeding exacerbated collagen deposition and further increased fibrosis-related gene expression in adipose tissue. Exercise attenuated or reversed these changes. Additionally, PPARγ, which has been shown to inhibit adipose tissue fibrosis, was observed to be increased following exercise. Moreover, exercise decreased the expression of HIF-1α in adipose fibrosis, and adipose tissue inflammation was inhibited. In conclusion, our data indicate that exercise attenuates and even reverses the progression of adipose tissue fibrosis, providing a plausible mechanism for its beneficial effects on glucose metabolism in obesity.
Department of Surgery, The University of Melbourne, Parkville, Victoria, Australia
Department of Urology, Royal Melbourne Hospital, Parkville, Victoria, Australia
Search for other papers by Stefano Mangiola in
Google Scholar
PubMed
Search for other papers by Ryan Stuchbery in
Google Scholar
PubMed
Department of Urology, Royal Melbourne Hospital, Parkville, Victoria, Australia
Search for other papers by Patrick McCoy in
Google Scholar
PubMed
Department of Urology, Royal Melbourne Hospital, Parkville, Victoria, Australia
Search for other papers by Ken Chow in
Google Scholar
PubMed
Australian Prostate Cancer Research Centre Epworth, Richmond, Victoria, Australia
Ontario Institute for Cancer Research, Toronto, Canada
Princess Margaret Cancer Centre, University Health Network, Toronto, Canada
Search for other papers by Natalie Kurganovs in
Google Scholar
PubMed
Search for other papers by Michael Kerger in
Google Scholar
PubMed
Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia
Department of Medical Biology, University of Melbourne, Melbourne, Victoria, Australia
Sir Peter MacCallum Department of Oncology, University of Melbourne, Melbourne, Victoria, Australia
Department of Mathematics and Statistics, University of Melbourne, Melbourne, Victoria, Australia
Search for other papers by Anthony Papenfuss in
Google Scholar
PubMed
Department of Urology, Royal Melbourne Hospital, Parkville, Victoria, Australia
Search for other papers by Christopher M Hovens in
Google Scholar
PubMed
Department of Urology, Royal Melbourne Hospital, Parkville, Victoria, Australia
Department of Urology, Frankston Hospital, Frankston, Victoria, Australia
Search for other papers by Niall M Corcoran in
Google Scholar
PubMed
Prostate cancer is a leading cause of morbidity and cancer-related death worldwide. Androgen deprivation therapy (ADT) is the cornerstone of management for advanced disease. The use of these therapies is associated with multiple side effects, including metabolic syndrome and truncal obesity. At the same time, obesity has been associated with both prostate cancer development and disease progression, linked to its effects on chronic inflammation at a tissue level. The connection between ADT, obesity, inflammation and prostate cancer progression is well established in clinical settings; however, an understanding of the changes in adipose tissue at the molecular level induced by castration therapies is missing. Here, we investigated the transcriptional changes in periprostatic fat tissue induced by profound ADT in a group of patients with high-risk tumours compared to a matching untreated cohort. We find that the deprivation of androgen is associated with a pro-inflammatory and obesity-like adipose tissue microenvironment. This study suggests that the beneficial effect of therapies based on androgen deprivation may be partially counteracted by metabolic and inflammatory side effects in the adipose tissue surrounding the prostate.