A Global Review of Obesity

Obesity is major health problem and are defined as abnormal or excessive amount of fat accumulation that presents a risk to health. A body mass index (BMI) over 24 is considered overweight, and over 30 is obese. obesity are main risk factors for a number of chronic diseases, like cardiovascular diseases such as heart disease and stroke, which are the leading causes of death worldwide. Over 800 million people around the world are living with obesity. The medical consequences of obesity will cost over $1 trillion by 2025. People living with obesity are twice as likely to be hospitalized if tested positive for COVID-19. The weight loss segments are one of the major contributors to the overall revenue of the dietary supplements in market. Anti-obesity drugs are used as pharmacological agents which reduce or control body weight. These drugs can change one of the fundamental processes of the human body or weight regulation by altering either appetite or absorption of calories. The treatment for obese patients is dieting and physical exercise. An anti-obesity drug have produce sustained weight loss with minimal side effects.

Understanding Obesity: How and Why?

Obesity is now recognised as a chronic disease which needs chronic treatment to treat or prevent obesity related complications. This article discusses the biology of weight regulation as a basis to understanding obesity as a disease, and to appreciate the complex and multifactorial nature of the obesity problem. Finally, the article highlights the dietary approaches as part of the multi-pronged approach to treating obesity and gives a brief update on intermittent fasting.

Mice lacking PC1/3 expression in POMC-expressing cells do not develop obesity

Pro-opiomelanocortin (POMC) neurons form an integral part of the central melanocortin system regulating food intake and energy expenditure. Genetic and pharmacological studies have revealed that defects in POMC synthesis, processing, and receptor signaling lead to obesity. It is well established that POMC is extensively processed by a series of enzymes, including prohormone convertases PC1/3 and PC2, and that genetic insufficiency of both PC1/3 and POMC is strongly associated with obesity risk. However, whether PC1/3-mediated POMC processing is absolutely tied to body weight regulation is not known. To investigate this question, we generated a Pomc-CreER T2; Pcsk1 lox/lox mouse model in which Pcsk1 is specifically and temporally knocked out in POMC-expressing cells of adult mice by injecting tamoxifen at eight weeks of age. We then measured the impact of Pcsk1 deletion on POMC cleavage to ACTH and α-MSH, and on body weight. In whole pituitary, POMC cleavage was significantly impacted by the loss of Pcsk1, while hypothalamic POMC-derived peptide levels remained similar in all genotypes. However, intact POMC levels were greatly elevated in Pomc-CreER T2; Pcsk1 lox/lox mice. Males expressed two-fold greater levels of pituitary PC1/3 protein than females, consistent with their increased POMC cleavage. Past studies show that mice with germline removal of PC1/3 do not develop obesity, while mice expressing mutant PC1/3 forms do develop obesity. We conclude that obesity pathways are not disrupted by PC1/3 loss solely in POMC-expressing cells, further disfavoring the idea that alterations in POMC processing underlie obesity in PCSK1 deficiency.