Exploring the Genetic Conception of Obesity via the Dual Role of FoxO

Abstract

Obesity or overweight are not superficial problems, constituting a pressing issue. The obesity index has almost tripled since 1975, which is an alarming state. Most of the individuals are currently becoming overweight or have inappropriate body mass index (BMI) conditions. Obesity is characterized by increased fat accumulation and thus poses a higher health risk. There is increased size and volume of fat cells in the body, which usually accounts for obesity. Many investigations have been carried out in this area, such as behavioral improvements, dietary changes, chemical involvements, etc., but presently no such goals are established to manage these health concerns. Based on previous literature reports and our interpretation, the current review indicates the involvement of various transcriptional and transporter functions in modifying the above-mentioned health conditions. Various transcriptional factors such as Forkhead box O1 (FoxO1) impart a significant effect on the physiology and pathology of metabolic dysfunction such as obesity. FoxO1 plays a dual role whether in the progression or suppression of metabolic processes depending on its targets. Thus, in the current study, will be discussed the dual role of FoxO1 in metabolic conditions (such as obesity), also summarizing the role of various other transcriptional factors involved in obesity.

Efficacy of Probiotic Strains Lactobacillus sakei Probio65 and Lactobacillus plantarum Probio-093 in Management of Obesity: An In Vitro and In Vivo Analysis

“…Obesity is a chronic condition and a complex disease reflected by an excessiveness of body fat, expanded adiposity, and altered cell composition of adipose tissues. Additionally, it is interconnected alongside an inflated risk of various health conditions, including high blood pressure, cardiac arrest, asthma, diabetes, and several types of cancer [ 1 , 2 , 3 , 4 ]. Adipose tissue (AT) is a metabolic body part that plays a crucial role in controlling energy homeostasis.…”

“…Numerous studies have demonstrated that obesity is often caused by the excessive consumption of high-fat diet (HFD) foods, leading to the expansion and alteration of fat cells, resulting in inflammation and oxidative stress [ 1 , 2 , 4 , 12 ]. Inflammation, closely associated with insulin resistance and metabolic dysregulation induced by obesity, can be effectively mitigated by selectively targeting and inhibiting key inflammatory pathways within AT [ 4 , 13 , 14 , 15 , 16 , 17 , 18 ].…”

Obesity control and liver health in breast cancer: Normalized hepatic elasticity after ketogenic diet

“…However, from a medically-monitored tool for treating epilepsy, it was converted to a mainstream dietary weight reduction option [ [6] , [7] , [8] , [9] ]. KD is a high-fat, low-carb, moderate-protein diet that produces metabolic changes leading to increased levels of free fatty acids and serum ketones and reduced blood insulin, glucose, and glucagon concentrations [ 6 , 10 ]. KD appears to create an unfavorable metabolic environment for the proliferation of breast cancer cells.…”

Anti-Obesity Drug Delivery Systems: Recent Progress and Challenges

“…When adipose tissue undergoes modifications due to adipocyte cell death, obesity is often accompanied by an increase in immune cells, particularly macrophages. These immune cells release pro-inflammatory proteins as cell signalling molecules, which contribute to the insulin resistance commonly observed in obese individuals [25]. Obesity is a treatable disease that can be managed by either physical or therapeutic control, as discussed briefly below.…”