Gut fat signaling and appetite control with special emphasis on the effect of thylakoids from spinach on eating behavior

Abstract

The metabolic controls of eating are embedded in a neural system that permits an interaction with the environment. The result is an integrated adaptive response that coordinates the internal milieu with the prevailing environment. Securing adequate amounts of fat and optimizing its storage and use has an evolutionary basis. By generating neuronal and endocrine feedback signals, behavior and metabolism could then adapt to fluctuations in food availability. However, in modern society, foods that appeal to the palate are neither in shortage nor are they difficult to procure. These foods can activate brain reward circuitry beyond their evolved 'survival advantage' limits. Many foods high in fat invoke an undeniably pleasurable sensation and could excessively stimulate the brain's reward pathways leading to overeating. However, the high appeal and potential for being eaten in excess notwithstanding, fat has the added distinction of inducing powerful signals in the gut that are transduced to the brain and result in the regulation of appetite. Fatty acids are sensed by G-protein-coupled receptors on enteroendocrine cells which trigger the release of peptides involved in appetite regulation. Lipid sensing may also occur through the fatty acid translocase, CD-36, on enterocytes. Additionally, fat can activate dopaminergic systems affecting reward, to promote an inhibition over eating. Prolonging the presence of fats in the gastrointestinal lumen permits the activation of signaling mechanisms. Thylakoids, found within the chloroplasts of plants, are flattened disc-like membranous vesicles in which the light-dependent reactions of photosynthesis occur. By interacting with lipids and delaying fat digestion, thylakoid membranes promote the release of peptides involved in appetite regulation and may influence the reward system. This review explores gut lipid sensing and signaling in the context of appetite regulation. The effects of thylakoid membranes on eating behavior are also reviewed.

A gut-derived hormone suppresses sugar appetite and regulates food choice in Drosophila

“…Such homeostatic nutrient consumption requires sensors that detect the internal nutritional state and mechanisms that translate this information into changes in feeding decisions. Food consumption is controlled by nutritional signals from the periphery, such as the adipokine leptin and a variety of gut hormones, that act together with circulating nutrients on the brain 7 . However, the hormones and mechanisms that govern nutrient-specific appetites that drive appropriate food choices to maintain or restore homeostasis are poorly defined.…”

Appethyl® and reduction of body weight: evaluation of a health claim pursuant to Article 13(5) of Regulation (EC) No 1924/2006

“…The applicant identified 10 publications as being pertinent to the claim. Five publications report on three human intervention studies (Montelius et al., 2014a ; Rebello et al., 2015a ; Stenblom et al., 2016 , 2015 ; Montelius et al., 2016 ), two publications report on animal studies (Montelius et al., 2014b ; Stenblom et al., 2016 ), one is a systematic review (Amirinejad et al., 2020 ) and two are narrative reviews (Rebello et al., 2015b ; Foshati and Ekramzadeh, 2020 ). The applicant also submitted two unpublished human intervention studies as being pertinent to the claim, claimed as proprietary by the applicant (Holtz et al., 2015 ; Postrach, 2021 ).…”

“…One narrative review (Foshati and Ekramzadeh, 2020 ) explored the potential effects and mechanism of action of thylakoids in general on overweight and obesity. The other narrative review (Rebello et al., 2015b ) evaluated the role of gut fat signalling in appetite control and focused on the potential impact of thylakoids derived from spinach on eating behaviour. These publications do not report additional experimental data on the effects of Appethyl® on body weight.…”

(Wh)olistic (E)ndocannabinoidome-Microbiome-Axis Modulation through (N)utrition (WHEN) to Curb Obesity and Related Disorders

“…The peculiar trait of anorectic OEA is very distinctive of cholecystokinin (CCK), as it works in a manner that, apart from reducing the meal size, also increases the latency period [ 67 ], providing it with a unique characteristic among the class of NAEs. Even though the consumption of C18:1n9 enriched food products manifolds the synthesis of OEA and its resulting benefits, the excessive intake of oils or high fats may hinder its production because of the disruption of the gut-brain axis [ 68 ]. Therefore, a thorough probe is mandatory to ascertain the compensatory limits of the ingestion of fats and oils.…”