Metabolic Syndrome and Overactive Bladder Syndrome May Share Common Pathophysiologies

Metabolic syndrome (MetS) is defined by a group of cardiovascular risk factors, including impaired glucose tolerance, central obesity, hypertension, and dyslipidemia. Overactive bladder (OAB) syndrome consists of symptoms such as urinary urgency, frequency, and nocturia with or without urge incontin...

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Bibliographic Details
Published in:Biomedicines 2022-08, Vol.10 (8), p.1957
Main Authors: Hsu, Lin-Nei, Hu, Ju-Chuan, Chen, Po-Yen, Lee, Wei-Chia, Chuang, Yao-Chi
Format: Article
Language:English
Subjects:
Atherosclerosis
Autonomic nervous system
Bladder
Body fat
Botulinum toxin
Cardiovascular disease
Cardiovascular diseases
Cholesterol
Diabetes
Dysbacteriosis
Dyslipidemia
Epidemiology
Fasting
Glucose
Glucose tolerance
Hyperplasia
Hypertension
Inflammation
Insulin
Insulin resistance
International organizations
Ischemia
Metabolic syndrome
microbiota
neuropathy
Nocturia
Nutrition research
Obesity
overactive bladder
Oxidative stress
Pathophysiology
Pelvis
Prostate
Quality of life
Review
Risk factors
Therapeutic targets
Urogenital system
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Summary:Metabolic syndrome (MetS) is defined by a group of cardiovascular risk factors, including impaired glucose tolerance, central obesity, hypertension, and dyslipidemia. Overactive bladder (OAB) syndrome consists of symptoms such as urinary urgency, frequency, and nocturia with or without urge incontinence. The high prevalences of metabolic syndrome (MetS) and overactive bladder (OAB) worldwide affect quality of life and cause profound negative impacts on the social economy. Accumulated evidence suggests that MetS might contribute to the underlying mechanisms for developing OAB, and MetS-associated OAB could be a subtype of OAB. However, how could these two syndromes interact with each other? Based on results of animal studies and observations in epidemiological studies, we summarized the common pathophysiologies existing between MetS and OAB, including autonomic and peripheral neuropathies, chronic ischemia, proinflammatory status, dysregulation of nutrient-sensing pathways (e.g., insulin resistance at the bladder mucosa and excessive succinate intake), and the probable role of dysbiosis. Since the MetS-associated OAB is a subtype of OAB with distinctive pathophysiologies, the regular and non-specific medications, such as antimuscarinics, beta-3 agonist, and botulinum toxin injection, might lead to unsatisfying results. Understanding the pathophysiologies of MetS-associated OAB might benefit future studies exploring novel biomarkers for diagnosis and therapeutic targets on both MetS and OAB.
ISSN:2227-9059
2227-9059
DOI:10.3390/biomedicines10081957