The Interplay of Vitamin D Deficiency and Cellular Senescence in The Pathogenesis of Obesity-Related Co-Morbidities.
Abdulhadi BimaBasmah Medhat EldakhakhnyDina NuwaylatiAbrar AlnamiMohammed AjabnoorAyman Zaky ElsamanoudyPublished in: Nutrients (2021)
This scoping review aims to clarify the interplay between obesity, vitamin D deficiency, cellular senescence, and obesity-related metabolic consequences, mainly subclinical atherosclerosis, and non-alcoholic fatty liver disease (NAFLD). Obesity is a significant global health problem that involves cellular, environmental, behavioral, and genetic elements. The fundamental cause of obesity throughout all life stages is an energy imbalance, and its consequences are countless and, foremost, very common. Obesity has been comprehensively studied in the literature given its association with low serum vitamin D, with many proposed mechanisms linking the two conditions. Moreover, markers of exaggerated cellular senescence have been proven to accumulate in obese individuals. Subclinical atherosclerosis initiates an early stage that ends in serious cardiac events, and obesity, low vitamin D, and senescent cells largely contribute to its associated chronic low-grade inflammation. Furthermore, NAFLD signifies the hepatic manifestation of metabolic syndrome, and studies have highlighted the important role of obesity, vitamin D deficiency, and cellular senescence in its development. Therefore, we outlined the most important mechanisms tying these conditions to one another.
Keyphrases
- metabolic syndrome
- insulin resistance
- weight loss
- type diabetes
- high fat diet induced
- weight gain
- low grade
- early stage
- dna damage
- adipose tissue
- cardiovascular disease
- bariatric surgery
- endothelial cells
- oxidative stress
- heart failure
- systematic review
- cardiovascular risk factors
- uric acid
- cell proliferation
- lymph node
- signaling pathway
- squamous cell carcinoma
- gene expression
- risk assessment
- cell death
- genome wide
- induced apoptosis
- left ventricular
- drug induced
- liver fibrosis
- life cycle
- neoadjuvant chemotherapy