Nutritional and Metabolic Diseases

Gland and Hormone Related Diseases

All Conditions

Symptoms and General Pathology

Neoplasms

Urinary Tract, Sexual Organs, and Pregnancy Conditions

Diabetes Mellitus

Syndrome

Prostatic Neoplasms

Obesity

Metabolic Syndrome

Metabolic Diseases

Hypogonadism

Eunuchism

Insulin Resistance

Hyperinsulinism

Glucose Metabolism Disorders

Gonadal Disorders

Endocrine System Diseases

All Drugs and Chemicals

Androgens

Testosterone

Hormones

Hormone Antagonists

20 Eugonadal Healthy men 20 Men with Testosterone Deficiency not currently on Testosterone replacement therapy

20 Men with Testosterone Deficiency progressed from OBS1 6 months post initiation of testosterone replacement therapy

20 men with prostate cancer planned for GnRH analogue therapy

In OBS1 20 men will be started on Testosterone replacement therapy as per routine clinical practice. Data collection will occur prior initiating therapy, and 6 months post

20 men in OBS2 planned for GnRH analogue therapy will undergo data collection prior, and 3 months post initiation of GnRH analogue therapy

GnRH

Michael O' Reilly, FRCPI PhD

Clare Miller, MBBS

Michael Professor O'Reilly, FRCPI PhD

Clare Dr Miller, BM BS

This study relates to men with hypogonadism, a condition describing a deficiency of androgens such as testosterone. Deficiency of these hormones occurs in men due to testicular (primary) or hypothalamic-pituitary (secondary) problems or may be observed in men undergoing androgen deprivation therapy for prostate cancer.

Testosterone plays an important role in male sexual development and health, but also plays a key role in metabolism and energy balance. Men with testosterone deficiency have higher rates of metabolic dysfunction. This results in conditions such as obesity, nonalcoholic fatty liver disease, diabetes, and cardiovascular disease. Studies have confirmed that treating testosterone deficiency with testosterone can reduce the risk of some of these adverse metabolic outcomes, however cardiovascular mortality remains higher than the general population. We know that testosterone deficiency therefore causes metabolic dysfunction. However, research to date has not established the precise mechanisms behind this.

In men with hypogonadism there is a loss of skeletal muscle bulk and function. Skeletal muscle is the site of many critical metabolic pathways; therefore it is likely that testosterone deficiency particularly impacts metabolic function at this site. Men with testosterone deficiency also have excess fat tissue, this can result in increased conversion of circulating hormones to a type of hormone which further suppresses production of testosterone. The mechanism of metabolic dysfunction in men with hypogonadism is therefore multifactorial.

The purpose of this study is to dissect the complex mechanisms linking obesity, androgens and metabolic function in men. Firstly, we will carry out a series of detailed metabolic studies in men with testosterone deficiency, compared to healthy age- and BMI-matched men. Secondly, we will perform repeat metabolic assessment of hypogonadal men 6 months after replacement of testosterone in order to understand the impact of androgen replacement on metabolism. Lastly, we will perform the same detailed metabolic assessment in men with prostate cancer before and after introduction of a drug which causes testosterone deficiency for therapeutic purposes.

Male hypogonadism occurs due to a deficiency of androgens such as testosterone due to either primary (testicular) or secondary (hypothalamic pituitary) pathology. The incidence of testosterone deficiency is likely to increase with more cancer survivors, opiate use, increased awareness and thus diagnosis of testosterone deficiency. Hypogonadism in males is an independent risk factor for the development of metabolic syndrome and is associated with increased prevalence of insulin resistance, type two diabetes, non-alcoholic fatty liver disease, visceral adiposity, and cardiovascular disease.

The relationship between hypogonadism and metabolic dysfunction is bidirectional with secondary hypogonadism documented in a large proportion of men with obesity without a testicular or central cause of androgen deficiency. A vicious cycle exists whereby increased adipose tissue in men with obesity results in depleting circulating testosterone stores due to increased aromatisation of testosterone to oestrogen and suppression of gonadotrophin mediated testosterone secretion via negative feedback. This perpetuates visceral adiposity in men with pre-existing metabolic dysfunction.

The hormonal impact of visceral adiposity plays a role in aggravating metabolic disease in men with hypogonadism however the initial metabolic perturbation causing obesity and metabolic disease in these men has not been established. It is probable skeletal muscle dysfunction is a major player. Skeletal muscle is the primary site for glucose uptake and utilisation and houses critical metabolic pathways such as oxidative phosphorylation in mitochondria. Men with hypogonadism experience loss of skeletal muscle bulk and function. Research has previously demonstrated that pathologic alterations in androgen exposure result in mitochondrial dysfunction in females. Studies have also confirmed improvements in mitochondrial function include increased phosphorylation of AMPKα in men with diabetes and hypogonadotropic hypogonadism and in animal models increased expression of genes related to mitochondrial respiration enzymes following introduction of testosterone(12). These findings hint at a pivotal role for androgens in mitochondrial function and energy biogenesis in skeletal muscle. However, to date no mechanistic study has established the precise cellular mechanisms adversely modified by androgen deficiency in males.

Induction of hypogonadism or medical castration is a well-established therapeutic goal in men with recurrent or metastatic hormonally driven prostate cancer. This is typically achieved with androgen deprivation therapy either a GnRH analogue or androgen receptor blockade. Over half of men receiving ADT for treatment of prostate cancer experience metabolic syndrome. These men represent an excellent biological model for studying the association between hypogonadism and metabolic syndrome however research to date has focused on establishing the association but not the responsible mechanisms.

This study will establish the mechanism of metabolic dysfunction in males with androgen deficiency. Firstly a cohort of men with hypogonadism prior to testosterone replacement will undergo detailed metabolic phenotyping using multiple approaches including metabolomic data from skeletal muscle samples, and metabolic parameters using serum samples. This data will be compared to age and weight matched eugonadal healthy controls before and after testosterone replacement as per routine clinical care. The same detailed metabolic phenotyping will be performed on men with prostate cancer before and after therapeutic induction of hypogonadism.

Our study will provide an unparalleled understanding of the tissue- and sex-specific role of androgens as a driver of metabolic dysfunction. Anticipated disturbances in mitochondrial function and energy biogenesis in androgen excess and deficiency will advance scientific knowledge and create potential for developing future tissue specific mediators of metabolic dysfunction in males with hypogonadism.

Serum Samples for targeted and non targeted metabolomics Saliva samples for targeted metabolomics Urine samples for targeted metabolomics Skeletal muscle samples for non targeted metabolomics

Exploring the Relationship Between Androgen Metabolism, Metabolic Disease and Skeletal Muscle Energy Balance in Men

Differences in non-targeted serum and skeletal muscle metabolomics in men with hypogonadism compared to controls

Differences in non-targeted serum and skeletal muscle metabolomics in men

Differences in steroid metabolomics in men with prostate cancer pre- and post-androgen deprivation therapy (ADT)

Differences in serum, urinary and salivary steroid metabolism

Steroid Metabolism Analysis Core, University of Birmingham

Institute of Systems, Molecular and Integrative Biology, University of Liverpool

Royal College of Surgeons, Ireland

Nervous System Diseases

Hypoxia

Brain Neoplasms

Central Nervous System Neoplasms

Nervous System Neoplasms

Brain Diseases

Central Nervous System Diseases

Signs and Symptoms, Respiratory

Central Nervous System Depressants

Analgesics

Pharmaceutical Solutions

Anesthetics

Dexmedetomidine

Hypnotics and Sedatives

Analgesics, Non-Narcotic

Adrenergic Agents

Adrenergic alpha-Agonists

Adrenergic Agonists

Neurotransmitter Agents

Dexmedetomidine 2 μg/ml will be given as bolus 1mg/kg for 10 minutes with a maintenance dose of 0.8μg/kg/h until surgery completion

Normal saline (NaCl 0.9%) administration will start 10 minutes after anesthesia induction and maintained throughout the surgical procedure.

Equivalent doses for a solution containing 2mcg/ml of the tested drug calculating for a bolus 1mg/kg for 10 minutes with a maintenance dose of 0.8μg/kg/h until surgery completion

Normal saline

Georgia Tsaousi, Professor

Brain tumor surgery is commonly associated with different degrees of preoperative intracranial hypertension and surrounding tumor edema, elicited by tumor underlying pathophysiology. During craniotomy for brain tumor resection maintenance of hemodynamic stability and intracranial homoeostasis is of paramount importance. Disordered hemodynamics or adverse stress may activate the immune inflammation or neuroendocrine responses and lead to a surge of inflammatory mediators and stress hormones, which are implicated in secondary brain insults.

Adverse physiological responses caused by intraoperative disordered hemodynamics or surgery-related damage, may lead to some secondary brain injury (such as cerebral edema or cerebral hemorrhage), aggravating damage to brain tissue and affecting the recovery from anesthesia, cognition and prognosis in patients.

Prevention of secondary brain injury is a key-endpoint to improve clinical outcomes in glioma patients undergoing craniotomy.

Alpha2-adrenoceptor agonists have been widely used for sedation, analgesia and anti-sympathetic actions for many years, but the definite evidence of their potential use as neuroprotectants has so far been confined to animal studies, yet the findings are inconsistent.

Dexmedetomidine (DEX) has been demonstrated to be a new type a2 adrenergic receptor (a2-AR) agonist, which can selectively bind with the a1 and a2 adrenergic receptor, and playing a dual role by restraining the activity of sympathetic nervous and stimulating the vagus nerve. Dexmedetomidine (DEX) also plays an important role in in inhibiting inflammatory and neuroendocrine responses. Animal experiments showed that the right must have a dexmedetomidine neuro-protective effect. However, the brain-protective effect of dexmedetomidine in anesthesia of craniotomy resection of glioma has not been reported.

Thus, the aim of this study was to explore the effect of dexmedetomidine on perioperative brain protection, as well as cerebral oxygenation and metabolic status aiming to provide a basis for clinical rational drug use in patients undergoing craniotomy resection of glioma.

Each participant will receive standard monitoring (ECG, SpO2, SBP, BIS, urine output, temperature). More detailed hemodynamic monitoring will be obtained by Edwards Lifesciences ClearSight system (CO, CI, SV, SVI, SVV, SVR, SVRI).

TCI Propofol and Remifentanil will be the agents of choice for induction and maintenance in anesthesia and cisatracurium will be used for neuromuscular blockade for intubation.

Protective mechanical ventilation will be chosen (7ml/kg IBW) with a respiratory rate to obtain a PaCO2 of 35-40 mmHg. PEEP will be changed for the best PaO2/FiO2 ratio and FiO2 of choice will be 0.5.

The radial artery catheterization will be applied for direct blood pressure measurement and arterial blood gas sampling (pH, PaO2, PaCO2, HCO3, BE, osmolality, lactic acid, Hb, glucose, Na and K will be measured).

The jugular bulb ipsilateral to the craniotomy site will be catheterized for receiving blood samples for blood gas analysis. The following oxygenation and metabolic parameters / derivates will be measured or calculated: SjvO2, pH, PjvO2, PjvCO2, HCO3, BE, Osmolality, Lactic acid jv, Hb, Glucose, Na, K, AjvDO2, AjvCO2, O2ERbr, eRQbr, AjvDL, and LOI.

Dexmedetomidine or normal saline (placebo) administration will start 10 minutes after anesthesia induction and maintained throughout the surgical procedure.

Phases

* T0: 5 minutes before administration of either DEX or placebo
* T15: 10 minutes after administration of either DEX or placebo
* T30: 30 minutes after administration of either DEX or placebo
* T60: 60 minutes after administration of either DEX or placebo
* T120: 120 minutes after administration of either DEX or placebo
* T240: 240 minutes after administration of either DEX or placebo
* End of surgical procedure Blood samples for measuring S-100b, NSE, cortisol, TNF-a and IL-6 will be obtained at phases T0, end of surgery and 24 hours after administration of either DEX or placebo.

Neurocognitive testing will be performed before surgery, 1 week and 1 month later using Karnofsky Performance Status (KFS), Mini Mental State Exam (MMSE), Μontreal Cognitive Assessment (MoCA) and Addenbrooke's Cognitive Exam (ACE III).

Intraoperative consumption of propofol and remifentanil will also be recorded

Effect of Dexmedetomidine on Brain Homeostasis and Neurocognitive Outcome

Effect of Dexmedetomidine on Brain Homeostasis and Neurocognitive Outcome of Patients Undergoing Brain Tumor Exclusion

Alterations in jugular venous oxygen saturation (%), after intravenous infusion of equivalent doses of dexmedetomidine or placebo (normal saline)

Alterations in arterio-jugular oxygen difference (AjvDO2 \[ml/dl\]), after intravenous infusion of equivalent doses of dexmedetomidine or placebo (normal saline)

Alterations in arterio-jugular carbon dioxide difference (AjvCO2 \[mmHg\]), after intravenous infusion of equivalent doses of dexmedetomidine or placebo (normal saline)

Alterations in brain oxygen extraction ratio (O2Erbr \[%\]), after intravenous infusion of equivalent doses of dexmedetomidine or placebo (normal saline)

Alterations in S-100b (μg/L) after intravenous infusion of equivalent doses of dexmedetomidine or placebo (normal saline)

Alterations in NSE (ng/ml) after intravenous infusion of equivalent doses of dexmedetomidine or placebo (normal saline)

Alterations in serum cortisol (μg/dl) levels after intravenous infusion of equivalent doses of dexmedetomidine or placebo (normal saline)

Alterations in serum TNF-a (pg/ml) levels after intravenous infusion of equivalent doses of dexmedetomidine or placebo (normal saline)

Alterations in serum IL-6 (pg/ml) levels after intravenous infusion of equivalent doses of dexmedetomidine or placebo (normal saline)

Alterations in Mini-Mental State Exam (MMSE) after intravenous infusion of equivalent doses of dexmedetomidine or placebo (normal saline)

Alterations in Μontreal Cognitive Assessment (MoCA) after intravenous infusion of equivalent doses of dexmedetomidine or placebo (normal saline)

Alterations in Addenbrooke's Cognitive Exam (ACE III) after intravenous infusion of equivalent doses of dexmedetomidine or placebo (normal saline)

Georgia Tsaousi

Assistant Professor

Diseases and Abnormalities at or Before Birth

Rare Diseases

Polycystic Ovary Syndrome

Hyperandrogenism

Cysts

Ovarian Cysts

Ovarian Diseases

Adnexal Diseases

Genital Diseases, Female

Genital Diseases

Urogenital Diseases

Female Urogenital Diseases

Pregnancy Complications

Female Urogenital Diseases and Pregnancy Complications

Disorders of Sex Development

46, XX Disorders of Sex Development

Congenital Abnormalities

Urogenital Abnormalities

Adrenal Hyperplasia, Congenital

Adrenogenital Syndrome

Male Urogenital Diseases

Congenital Adrenal Hyperplasia

21-hydroxylase Deficiency

Xiu Qiu, PhD

Zehong Zhou, MD

The Offspring Born to Mothers with Polycystic Ovary Syndrome in Guangzhou Cohort study (PCOS-BIG) was established to investigate the short- and long-term effects of intrauterine exposure to maternal PCOS on the health of offspring in Guangzhou, China. Data are collected regarding maternal PCOS subtypes, nursing, diet and education as well as health outcomes in their later life. Biological samples including blood and tissue samples are also collected from participants.

According to preliminary survey, the prevalence of polycystic ovary syndrome (PCOS) among Chinese women reached 7.5%. Hyperandrogenism and insulin resistance were considered as the main pathogenesis of PCOS. As reported, the secretion of androgen is higher among women with PCOS than the healthy reference population throughout their fertile lives. Worth of concern, offspring of PCOS patients presented with glucolipid metabolism disorders as early as during their childhood, while whose pathogenesis remains unclear. Prenatal exposure of rhesus monkey in pregnant to androgens produces glucolipid metabolic alterations in offspring resembling those in PCOS, suggesting that the exposure of the fetus to hyperandrogenism during gestation could affect the glucolipid metabolism of PCOS offspring. Growing evidence shows that different exposures during pregnancy will affect the DNA methylation of offspring and disturb their endocrine and metabolism. A birth cohort would provide an opportunity to examine the short- and long-term effects of PCOS exposure, such as hyperandrogenism, on health consequences of the offspring.

During pregnancy: maternal blood, urine and stool. At delivery: cord, cord blood and placenta. During Infancy：dry blood spot, stool and blood. During childhood:blood, buccal swab and stool.

Offspring Born to Mothers With Polycystic Ovary Syndrome in Guangzhou Cohort Study

Health of Offspring Born to Mothers With Polycystic Ovary Syndrome in Guangzhou Cohort Study

Participants with one or more abnormal laboratory values will be considered as with glucolipid metabolism disorder.

Assessed by self-reported time of onset and electronic medical records

Profiling DNA methylation and histone acetylation etc., using cord blood samples

Weight changes from birth, to age of 6 weeks, 6 months, 1 year, 3 years, 6 years, 12 years and 18 years old

Height changes from birth, to age of 6 weeks, 6 months, 1 year, 3 years, 6 years, 12 years and 18 years old

Assessed using Gesell Developmental Schedules, including five items of adaptive, gross motor, fine motor, language, and social function

Assessed using Dual Energy X-Ray Absorptiometry

Assessed using Peabody Picture Vocabulary Test (PPVT) and Raven's Standard Progressive Matrices (SPM). Of whom the score of PPVT ≥ 85 and the score of SPM ≥ 90, the child will be considered as normal level of intelligence quotient and of whom the score of PPVT under 85 or the score of SPM under 90 will be considered as suspected lower intelligence quotient.

Child screened as of suspected lower intelligence quotient will be assessed by Wechsler Preschool and Primary Scale of Intelligence-Fourth edition (WPPSI-IV), including 5 items: verbal comprehension, visual spatial, fluid reasoning, working memory and process speed. Scores of the five items are added to get the total score.

Assessed by assay of hormones, including follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), total testosterone (TT), free testosterone (FT), androstenedione (A4), dehydroepiandrosterone sulfate (DHEA-S) and sex hormone binding globulin (SHBG), and by acne scoring and hirsutism scoring (modified Ferriman-Gallway scoring system). Participants with one or more abnormal laboratory values, and/or acne score ≥ 1, and/or hirsutism score ≥ 5 will be considered as with reproductive endocrine disorder.

University of Birmingham

Guangzhou Women and Children's Medical Center

Director of the Born in Guangzhou Cohort Study

Skin and Connective Tissue Diseases

Breast Neoplasms

Other Dietary Supplements

Benzocaine

Tannic Acid

Participants will be asked to follow a standardized 16:8 TRE protocol with an 11 am to 7 pm eating window for 16 weeks. Participants receive support to follow the TRE intervention from the study team which will include an initial consultation with a registered dietitian and ongoing tailored feedback via brief support calls from study staff at weeks 1, 3, 6, and 12.

Participants will be asked to follow a standardized 16:8 TRE protocol with an 11 am to 7 pm eating window for 16 weeks. Each participant will be matched with another participant in the same group to provide peer-based support to adhere to TRE. Study staff will introduce pairs and provide an introduction to TRE and then pairs will meet by phone/video at weeks 1, 3, 6, and 12 at a minimum, with additional contact encouraged.

Participants will be asked to follow TRE for 16 weeks with a protocol that is personalized to their preferences within the following pre-specified rules: 1) 8-10 hour eating window; 2) self-selected eating window start time as long as it ends ≥3h before bedtime; 3) if days off are required, aim to do so after following TRE for ≥5 successive days each week. Participants receive support to follow the TRE intervention from the study team which will include an initial consultation with a registered dietitian and ongoing tailored feedback via brief support calls from study staff at weeks 1, 3, 6, and 12.

Participants will be asked to follow TRE for 16 weeks with a protocol that is personalized to their preferences within the following pre-specified rules: 1) 8-10 hour eating window; 2) self-selected eating window start time as long as it ends ≥3h before bedtime; 3) if days off are required, aim to do so after following TRE for ≥5 successive days each week. Each participant will be matched with another participant in the same group to provide peer-based support to adhere to TRE. Study staff will introduce pairs and provide an introduction to TRE and then pairs will meet by phone/video at weeks 1, 3, 6, and 12 at a minimum, with additional contact encouraged.

Participants will be asked to maintain their usual diet and physical activity patterns for 16 weeks. They will receive the same number and timing of calls from study staff as the other groups (at randomization, 1, 3, 6, 12 weeks).

A standardized 16:8 TRE protocol with an 11 am to 7 pm eating window.

Standardized TRE Protocol

A personalized TRE protocol following pre-specified rules: 1) 8-10 hour eating window; 2) self-selected eating window start time as long as it ends ≥3h before bedtime; 3) if days off are required, aim to do so after following TRE for ≥5 successive days each week.

Personalized TRE Protocol

External support (from study staff) that includes consultation with a registered dietitian and ongoing tailored feedback via support calls at weeks 1, 3, 6, and 12.

External Support for TRE

Matched pairs will meet by phone/video at weeks 1, 3, 6, and 12.

Peer Support for TRE

Amy A Kirkham, PhD

This study will evaluate the implementation and effectiveness of free-living TRE on biological and behavioural breast cancer risk factors.

TRE is an eating pattern where individuals consume ad libitum energy intake within a set window of time, commonly 8 hours, which induces a fasting window of 16 hours per day (i.e., 16:8 TRE). TRE is a simple and accessible lifestyle intervention with high adherence potential that may target both biological and behavioural mechanisms of breast cancer risk.

Remote Time-restricted EAting DeliverY

Proof-of-Concept of Time-Restricted Eating as a Novel Lifestyle Intervention for Breast Cancer Prevention

Evaluated via the Hospital Anxiety and Depression Scale (HADS); This 14-item questionnaire has a minimum score of 0 and maximum of 21, where a higher score is worse.

Assessed daily through twice daily automated text messages asking participants to respond with what time they started and stopped eating that day.

Homeostatic Model Assessment for Insulin Resistance calculated as fasting glucose in mmol/l\*fasting insulin in μU/ml/22.5

Participants will be provided with a Dexcom G6 continuous glucose monitor transmitter and sensor. This data will be evaluated as the 5-day average of: 24-hour, daytime, and nocturnal glucose concentration, time in hyper, normo and hypoglycemia, and glycemic variability

Measured via venipuncture and core lab lab analysis

Measured via Fitbit Aria Air scale at baseline and 16-weeks but also once per week to evaluate trajectory of change

Measured via provided circumference measuring tape as the average of 2 measurements

Participant will be provided with a Bios 3al1-3e blood pressure measuring device. After 5 minutes of quiet seated rest, blood pressure will be measured 6 times, 60 seconds apart in a standardized seated position with the average of the 2nd through 6th measurement used.

Calculated via both the Framingham and Reynolds 10-year CVD risk scores using measured collected for study purposes (i.e., age, total cholesterol, HDL, systolic blood pressure, smoking status, C-reactive protein, family history of heart disease).

As defined by the NCEP/ATP III criteria using measurements taken using provided study tools

As defined by the NCEP/ATP III criteria and age and ethnic specific calculations

Evaluated via an 'End of Study Survey' (including a Diet Satisfaction Score Tool and acceptability questions) and semi-structured qualitative interviews

Evaluated as uptake of each delivery model, defined as adherence to the intervention touch points (i.e., external support: support calls with staff; peer support: number of peer interactions; both: response rate to adherence).

Intervention costs will be evaluated and averaged per participant from the time required for intervention phone calls, scheduling, and technical support for adherence app by the study staff according to hourly rates of pay.

Evaluated via participant self-report of continued TRE post-intervention

Measured via experience of selected relevant Common Terminology Criteria for Adverse Events (CTCAE v5) with additional questions about duration and change in the revised 18-item version of the Three-Factor Eating Questionnaire (aka Eating Inventory)

Measured by the RAND-36 Physical Component Summary. Physical component summary of the RAND-36 questionnaire (minimum = 0, maximum = 50, a higher score is a better outcome)

Measured via FitBit Inspire 2 as 7-day average

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
Exploring the Relationship Between Androgen Metabolism, Metabolic Disease and Skeletal Muscle Energy Balance in Men	NCT05773183	Hypogonadism, M... Testosterone De... Prostate Cancer Androgen Defici... Metabolic Disea... Metabolic Syndr... Metabolic Distu... Obesity Cardiovascular ... NAFLD Diabetes	Testosterone GnRH	18 Years - 60 Years	Royal College of Surgeons, Ireland
Effect of Dexmedetomidine on Brain Homeostasis and Neurocognitive Outcome	NCT04266665	Brain Tumor Metabolic Distu... Inflammatory Re... Oxygen Deficien...	Dexmedetomidine Normal saline	18 Years - 80 Years	Aristotle University Of Thessaloniki
Offspring Born to Mothers With Polycystic Ovary Syndrome in Guangzhou Cohort Study	NCT03742011	PCOS Offspring, Adul... Hyperandrogenis... Epigenetics Insulin Resista... Endocrine Disor... Metabolic Distu...		- 18 Years	Guangzhou Women and Children's Medical Center
Remote Time-restricted EAting DeliverY	NCT05454943	Metabolic Distu...	Standardized TR... Personalized TR... External Suppor... Peer Support fo...	50 Years -	University of Toronto
Exploring the Relationship Between Androgen Metabolism, Metabolic Disease and Skeletal Muscle Energy Balance in Men	NCT05773183	Hypogonadism, M... Testosterone De... Prostate Cancer Androgen Defici... Metabolic Disea... Metabolic Syndr... Metabolic Distu... Obesity Cardiovascular ... NAFLD Diabetes	Testosterone GnRH	18 Years - 60 Years	Royal College of Surgeons, Ireland
Remote Time-restricted EAting DeliverY	NCT05454943	Metabolic Distu...	Standardized TR... Personalized TR... External Suppor... Peer Support fo...	50 Years -	University of Toronto

Spots Global Cancer Trial Database for metabolic disturbance