Obesity and industry chemicals: more proofs mount evidences on lipid profiles

Until recently, scientists thought that diseases such as obesity and fatty liver resulted from anomalies in the metabolism of lipids triggered by excessive energy intake, fat consumption and lack of physical activity. Previous studies have provided strong evidence linking some hormone-like compounds to obesity in humans, but this is the first study that showed a cellular and metabolic effect on human cells exposed directly to those compounds. But a study published in the international journal Toxicology and Applied Pharmacology, highlights the existence of chemical compounds people are exposed to via a variety of consumer products. These can lead to fat-related metabolic diseases and weight gain. Chemical compounds found in many consumer products could be major contributors to the onset of obesity in humans. Ramon Lavado, PhD, assistant professor of Environmental sciences at Baylor University, with his team has been conducting experiments to determine whether their suspicion that obesogens — specific chemical compounds found to disrupt normal metabolic processes — promoted a dysregulation of lipid profiles in the human liver.

While poor nutrition and lack of exercise are known contributors to obesity, significant attention has emerged regarding the potential effects of some chemical compounds to trigger lipid-related diseases. Exposures to obesogens — particularly in early development in life — were found to disrupt normal metabolic processes and increase susceptibility to weight gain across the lifespan. As of the year 2000, there were an estimated 100,000 commercially available chemicals around the world. Two decades later, that amount has more than tripled, with approximately 350,000 chemicals being available, according to recent research published in the journal Environmental Science & Technology. Contributing chemicals to the diseases may be found in cigarette smoke, air pollution, pesticides, fungicides, flame retardants and a certain class of chemicals used in many consumer products to make them softer. Other contributors widely used in the past may have been industrial chemicals in cements, sealants, adhesives, paints, common plastics and fluorescent light ballast.

For the study, the team used well-established techniques in the field of metabolomics and molecular toxicology to investigate whether the proportion of lipids related to diseases, such as obesity, was modified upon exposure to environmental obesogens — and if so, to what extent the lipid profile changed. Additionally, they used a technique called fluorescence microscopy to investigate whether environmentally relevant concentrations of the tested compounds had the ability to induce fat accumulation in liver tissue. The chemicals rosiglitazone, tributyl-tin, di-2-ethylexylphthalate and perfluorooctanoic acid significantly increased total lipids in liver cells, the most prominent being diglycerides, triglycerides and phosphatidylcholines. Contrarily, perfluorooctane sulfonic acid and the drug fenofibrate lowered total lipids, especially those belonging to the triglycerides, acylcarnitine, ceramide and lecithin groups. Fluorescence microscopy analysis for cellular neutral lipids revealed significant lipid bioaccumulation upon exposure to obesogens at environmentally relevant concentrations. 

Another novel finding was that those effects were observed in cells exposed to chemical concentrations that are often seen in the environment and to which people are exposed constantly. This study is among the few that report molecular and physical changes at the cellular level, and the quantification of specific types of lipids that emerge as a result of chemical exposure. It is relevant to point that rosiglitazone is a common medication employed in the management of type 2 diabetes. According to the aforementioned results, rosiglitazone may be able to correct blood glucose homeostasis, but would predispose to fatty liver condition. Dr Lavado concluded: ” Additionally, study results strongly support the use of animal alternatives with more human relevance as a valuable tool in the characterization of health effects caused by chemicals for which humans are often exposed but lack thorough toxicological data. In the case of fat profile alterations, the idea that chemical compounds may trigger and/or contribute to the development of lipid-related diseases deserves extensive research in the future”.

  • Edited by Dr. Gianfrancesco Cormaci, PhD; specialist in Clinical Biochemistry.

Scientific references

Franco ME et al. Toxicol Appl Pharmacol 2020 Apr 27; 398:115009.

Dallio M et al. Int J Environ Res Public Health 2019 Aug; 16(17):3134. 

Kim JT, Lee HK. Ann Pediatr Endocrinol Metab 2017; 22(4):219-225. 

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Informazioni su Dott. Gianfrancesco Cormaci 2227 Articoli
- Laurea in Medicina e Chirurgia nel 1998 (MD Degree in 1998) - Specialista in Biochimica Clinica nel 2002 (Clinical Biochemistry specialty in 2002) - Dottorato in Neurobiologia nel 2006 (Neurobiology PhD in 2006) - Ha soggiornato negli Stati Uniti, Baltimora (MD) come ricercatore alle dipendenze del National Institute on Drug Abuse (NIDA/NIH) e poi alla Johns Hopkins University, dal 2004 al 2008. - Dal 2009 si occupa di Medicina personalizzata. - Detentore di un brevetto sulla preparazione di prodotti gluten-free a partire da regolare farina di frumento immunologicamente neutralizzata (owner of a patent concerning the production of bakery gluten-free products, starting from regular wheat flour). - Autore di un libro riguardante la salute e l'alimentazione, con approfondimenti su come questa condizioni tutti i sistemi corporei. - Autore di articoli su informazione medica, salute e benessere sui siti web salutesicilia.com e medicomunicare.it
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