Aim and Hypothesis
Obesity and its impact on the cardiovascular system are one of the central issues discussed in up-to-date medicine. The increased amount of fat tissue leads to such disorders as heart insufficiency, angina pectoris, atherosclerosis, heart attack, thromboembolism of pulmonary artery, and many others (Lv et al., 2018, p. 11). A substantial number of researchers tried to find ways to control the pro-inflammatory markers and hormones produced in adipose tissue to decrease the appetite and inflammation damaging the heart, vessels, and worsening human’s BMI (Gupta et al., 2021, p. 2). It was scientifically proved that a high level of ghrelin, a peptide hormone secreted by cells in the gastric fundus, leads to an increased appetite and subsequent weight gain (Makris et al., 2017, p. 1047; Zhang et al., 2017, p. 123). On the other side, adipose tissue starts expressing a variety of pro-inflammatory agents causing a cascade of damaging effects on systems and organs.
Some works focused on studying the effect of ghrelin on pro-inflammatory agents and molecules trying. One of the central pro-inflammatory molecules is TNF-α which is expressed by adipocytes. The authors tried to prove that ghrelin decreases the unwanted damaging effects of TNF-α that consequently prevents hepatocyte autophagy (Ezquerro et al., 2019, p. 23; Ezquerro, Frühbeck and Rodríguez, 2017, p. 405). The current research aims to continue the search for the positive ghrelin effects on the human cardiovascular system in connection with TNF-α.
The current study aims to analyze the effect of treatment time on the expression of TNF-α by treating 3T3-L1 differentiated adipocytes with ghrelin for 24 hours. The hypothesis is to prove the decrease of TNF-α concentration after ghrelin implementation on adipose cells. The null hypothesis can be the increase or no change of TNF-α concentration after the 24-hour addition of ghrelin. If the main hypothesis is proven right, then patients with comorbidities (both cardiovascular disease and obesity) can be treated with ghrelin to decrease inflammasome effects of TNF-α.
Method
The research method is experimental in the laboratory using differentiated cells for the investigation. The study is quantitative with the measurement of the concentration of the pro-inflammatory molecule before and after adding the hormone. 3T3-L1 is the line of adipocytes that was cultured and differentiated from embryonic mouse cells. These cells are imitating the functions of human adipocyte cells and have been used in multiple studies. The method involves 3T3-L1 cells that are put in a flask where later ghrelin is added for ten nm concentration. To assess further effects of ghrelin, the flask is left for twenty-four hours. The authors of the current work take the responsibility for the management of the procedure, collection, and measurement of the TNF-α marker expression. The measurement involves the tool enzyme-linked immunosorbent assay (ELISA). To estimate the concentration level of TNF-α before and after ghrelin, ELISA will be implemented in twenty-four hours.
If ELISA shows the decrease of TNF-α, it can be a new era in medical treatment for patients having both cardiovascular disease and obesity. If ELISA shows the increase of TNF-α, then the inflammation by all the actions raises which leads to a more damaging effect on tissues and organs. Hypothetically, ghrelin has various effects correlating with the reward system in the brain, leptin hormone, and appetite deviations. By studying some effects of ghrelin with new insights to the mechanism of action in the rewarding and motivational control, in the decrease of aggressive agents causing inflammation, an innovative methodology can lead to successful treatment and management of patients. A new indication of potential treatment can lead to promising outcomes in the prevention of severe cardiovascular pathologies.
Reference List
Al Massadi, O. et al. (2019) ‘Ghrelin and food reward’, Neuropharmacology, 148, pp. 131-138.
Ezquerro S., Frühbeck G. and Rodríguez A. (2017) ‘Ghrelin and autophagy’, Current Opinion in Clinical Nutrition and Metabolic Care, 20(5), pp. 402-408.
Ezquerro, S. et al. (2019) ‘Ghrelin reduces TNF-α-induced human hepatocyte apoptosis, autophagy and pyroptosis: role in obesity-associated NAFLD. The Journal of Clinical Endocrinology & Metabolism, 104(1), pp. 21-37.
Gupta, D. et al. (2021) ‘A LEAP 2 conclusions? Targeting the ghrelin system to treat obesity and diabetes’, Molecular Metabolism, 46, pp. 1-12.
Lv, Y. et al. (2018) ‘Ghrelin, a gastrointestinal hormone, regulates energy balance and lipid metabolism’, Bioscience Reports, 38 (5), pp. 1-23.
Makris, M. C. et al. (2017) ‘Ghrelin and obesity: identifying gaps and dispelling myths. A reappraisal’, In Vivo, 31(6), pp. 1047-1050.
Zhang, S. et al. (2017) ‘Elevated serum levels of ghrelin and TNF-α in patients with cyanotic and acyanotic congenital heart disease’, World Journal of Pediatrics, 13(2), pp. 122–128.