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Science deals with obesity on the table: sharing pleasures for coffee, tea and cocoa

Obesity and public health

There are not only infectious pandemics: obesity has become a significant public health problem worldwide due to its gradually increasing prevalence. The condition can potentially increase the risk of various health complications, including cardiovascular disease, diabetes, hypertension, atherosclerosis, and inflammatory metabolic diseases. Drugs used to treat obesity, such as sympathomimetics, serotonergic agonists, lipase inhibitors, cannabinoid receptor antagonists, and gastrointestinal-derived peptides, often fail to provide optimal benefits and are associated with many harmful side effects.

Coffee, tea and cocoa are the most used plant-based drinks with potential anti-obesity effects. Several studies have highlighted the effectiveness of the bioactive compounds present in these drinks in preventing obesity. The bioactive compounds present in coffee, tea and cocoa can inhibit white adipogenesis and promote brown adipogenesis and lipolysis, preventing obesity. While some compounds, including caffeine and chlorogenic acid, are present in all three drinks, some are specific to each type. Some of these specific compounds are trigonelline and cafestol in coffee, theaflavins and thearubigins in tea, and theobromine and quercetin in cocoa.

How coffee works in obesity

The main anti-obesity compounds found in green and roasted coffee include caffeine, chlorogenic acid, trigonelline, cafestol and kahweol. Existing evidence indicates that caffeine may increase metabolic rate and promote the breakdown of adipose tissue, resulting in reduced body weight. Caffeine may also increase fat oxidation during submaximal exercise. Evidence also indicates that it promotes thermogenesis by upregulating uncoupling proteins, increases lipolysis by increasing catecholamine secretion, inhibits lipogenesis, suppresses appetite, and reduces inflammatory responses. Studies investigating caffeine’s mode of action have found that it influences the AKT/GSK3β pathway and inhibits the expression of adipogenic proteins during adipocyte maturation.

Existing evidence on the health benefits of caffeine indicates that this bioactive compound can prevent obesity and non-alcoholic fatty liver disease. Caffeine and epigallocatechin-3-gallate (EGCG) have been found to work synergistically to prevent obesity. Studies investigating the mode of action of chlorogenic acid (CLOG) find that the compound can improve body weight, lipid metabolism and obesity-related hormone levels in mice eating high-fat diets. CLOG can inhibit fat accumulation by regulating the activities of enzymes related to hepatic lipid metabolism and can promote brown adipogenesis by activating the protein kinase AMPK. CLOG and caffeine synergistically promote brown adipogenesis through pathways mediated by AMPK and PPARα/γ receptors.

CLOG has also been found to prevent obesity by modulating the composition of the gut microbiota. Regarding trigonelline, however, this simple alkaloid (second in abundance in coffee) prevents obesity by increasing the insulin sensitivity index and decreasing lipid levels. Mechanistic studies have shown that trigonelline promotes brown adipogenesis by stimulating the p38 MAPK/ATF-2 signaling pathway and prevents excessive hypertrophy of white adipocytes. The actions of these substances are complemented by the most important diterpenoids which are cafestol and kahweol. Cafestol has been found to exert anti-obesity effects by increasing fat oxidation and energy expenditure. Regarding kahweol, evidence indicates that the compound inhibits adipogenesis by activating the AMPK pathway.

Tea in the management of obesity

Compounds with anti-obesity activity in tea include catechins, L-theanine, theaflavin, thearubigin, and theabrownin. It has been discovered that tea extracts prevent obesity by increasing brown adipogenesis, inhibiting white adipogenesis, increasing energy expenditure and inhibiting lipid synthesis. Mechanistic studies have found that EGCG in tea prevents adipogenesis by inducing cell cycle arrest in adipocytes. It also inhibits pancreatic lipase, salivary alpha-amylase and intestinal alpha-amylase which degrades dietary starch. Other modes of anti-obesity action of EGCG include increasing fecal excretion of fatty acids and inhibiting enzymes related to lipogenesis.

Another tea-derived compound, theaflavin, has been found to improve glycolipid metabolism and obesity by activating the SIRT6/AMPK/SREBP-1/FAS cell signaling pathway. The ultimate effect is the inhibition of fatty acid synthesis mediated by the FAS enzyme both at the liver and adipose tissue level. Other tea-derived compounds, including thearubigin and theabrownin, have been found to exert anti-obesity activity by increasing adipogenesis, improving blood lipid profile and reducing inflammatory cytokines. A final effect of tea polyphenols is to remodel the metabolic activity of the intestinal microbiota.

How does cocoa affect fat accumulation?

Cocoa polyphenols, including flavanols (epicatechin, catechin, and procyanidins), the flavonoid quercetin, anthocyanins, phenolic acids, and stilbenes, are known to have anti-obesity activities. Cocoa polyphenols have been found to exert anti-obesity effects by increasing energy expenditure and thermogenesis, improving blood lipid profile, and reducing oxidative stress and inflammation. Results from animal studies have shown that cocoa extracts can reduce blood cholesterol levels, regulate glucose metabolism and inhibit visceral adiposity. The main targets of cocoa polyphenols in carrying out this phenomenon are (peroxisomal) receptors (PPARs), liver X receptors (LXR-alpha), adiponectin genes and mitochondrial uncoupling proteins.

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

Scientific references

Wang Q. Curr Res Food Sci. 2024; 2024:100741.

Quiroz ES et al. Curr Res Food Sci. 2023; 7:100594.

Simpson EJ et al. Nutrients. 2023 Jan; 15(3):565.

Sun M et al. J Nutr Biochem. 2021 Jun; 92:108618.

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Dott. Gianfrancesco Cormaci
Dott. Gianfrancesco Cormaci
Laurea in Medicina e Chirurgia nel 1998; specialista in Biochimica Clinica dal 2002; dottorato in Neurobiologia nel 2006; Ex-ricercatore, ha trascorso 5 anni negli USA (2004-2008) alle dipendenze dell' NIH/NIDA e poi della Johns Hopkins University. Guardia medica presso la casa di Cura Sant'Agata a Catania. Medico penitenziario presso CC.SR. Cavadonna (SR) Si occupa di Medicina Preventiva personalizzata e intolleranze alimentari. Detentore di un brevetto per la fabbricazione di sfarinati gluten-free a partire da regolare farina di grano. Responsabile della sezione R&D della CoFood s.r.l. per la ricerca e sviluppo di nuovi prodotti alimentari, inclusi quelli a fini medici speciali.

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