Hunger hormones like Leptin (appetite-decreasing)+ghrelin (appetite-increasing)+other appetite hormones like GLP1/incretins - directly dealing with them?

[Alex K Chen]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6426280/

peptide YY acts to reduce food intake

Leptin can increase oxidative stress, though higher levels in DNAm leptin seem to be "a good thing" (this is entirely consistent)

Ghrelin is the appetite-increasing hormone, and decreasing its levels seems to be "better" than increasing leptin. I wonder if stimulants go after it. Semaglutide mostly lowers ghrelin

https://www.google.com/books/edition/Appetite_and_Food_Intake/JTclDwAAQBAJ?hl=en&gbpv=1&dq=ghrelin+leptin&printsec=frontcover

https://www.google.com/books/edition/The_Hungry_Brain/MVkODQAAQBAJ?hl=en&gbpv=1&dq=leptin+ghrelin&printsec=frontcover

I've had too many nut binges as of late, and eating til I'm full, and this has increased my calorie intake to non-ideal levels (esp b/c I'm impulsive/neurotic and want relief from hunger *now* to focus) - I have zero feedback loops but then this really risks that I suddenly lose my youth before I'm ready for it (this is what I really fear near-term, because I still need all the extra time)....

[anyways i found semaglutide just in time to save me]

 

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Water consumption may have direct effects on hunger hormones (Clark 2013). These are defined as ghrelin, leptin, insulin, cholecystokinin (CCK) and glucagon‐like peptide‐1 (GPL‐1). The effects are described in Mattes 2010. Ghrelin increases appetite by signalling hunger to the brain and is released primarily in the stomach. Leptin is an appetite suppressant made by fat cells. Insulin is made in the pancreas to enable the body to metabolise sugar (glucose) from carbohydrates and when there is an imbalance this can affect hunger levels. Cholecystokinin stimulates the digestion of fat and protein. GLP‐1 is produced in the gut and released in response to food where it stimulates insulin secretion and inhibits glucagon secretion and this contributes to feelings of satiety (Mattes 2010). Drinking extra water may rate limit the biochemical steps needed to metabolise fat because the glycaemic and insulin index of water is zero. This simplifies the fat breakdown of free fatty acids and the transport of these free fatty acids into the mitochondria where fat is oxidised. Drinking water rather than orange juice was noted to increase fat oxidation in normal weight individuals following a breakfast when tested on two consecutive days, even when they consumed more calories than they expended and engaged in no other intervention to reduce the calorie balance (Stookey 2012). Two days is not enough time to conclude that extra water intake is effective as a weight loss tool, however it is a promising observation.

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Semaglutide improved leptin sensitivity and anorexigenic signaling but lessened orexigenic signaling

https://journals.physiology.org/doi/full/10.1152/ajpgi.2001.281.3.G752 -  acarbose might increase incretins on carb-containing meals too...

Edited March 11 by InquilineKea

[Alex K Chen]

Sparkling water?!?!?

https://www.uclahealth.org/news/study-links-drinking-carbonated-water-and-weight-gain

Another found the exact opposite. It's unclear what the effects are on me

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The researchers also looked at the effects of sparkling water in humans. They had 20 men drink carbonated or plain water, and the results matched those of the rodent study. The men who drank either unsweetened or artificially sweetened carbonated water had triple the blood levels of ghrelin as those who drank plain water or degassed sparkling water. The study rotated the four beverages among all of the participants, so, by the end of the study, each man had partaken of each beverage. They concluded that the presence of carbon dioxide led to an increase in ghrelin production. 

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Total ghrelin, GIP and active GLP1 and visual analog scale (VAS) were measured over 4 h. Ghrelin was reduced greater after MUFA compared to PUFA at the beginning of the meal (at 30 and 60 min) and was significantly negatively correlated with subjective VAS for preoccupation for both MUFA and PUFA meals. No significant difference for ghrelin 240 min incremental area under the curve (iAUCs) were found. MUFA induced higher GIP response than PUFA. GIP was associated with all the VAS measurements except preoccupation for MUFA meal. No difference was found for GLP1 between two meals, nor was GLP1 associated with VAS. In conclusion, the results demonstrate that ghrelin, GIP and VAS respond differently to MUFA and PUFA meals. Ghrelin and GIP, but not GLP1, were associated with acute appetite control, especially after MUFA meal.

 

Edited November 12, 2023 by InquilineKea

[Alex K Chen]

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The cGMP signaling pathway is involved in many essential functions; it regulates phototransduction in the eyes, hypertension, reproduction, attention and hyperactive behavior, vasodilation, circadian rhythms, intestinal homeostasis, and cancer progression (Januszewicz 1995, Oster et al. 2003, Yau and Hardie 2009, Francis et al. 2010, Zhang et al. 2010, Gong et al. 2011, Arshad and Visweswariah 2012, Kim et al. 2013). In addition, it regulates body size, exploratory behavior, stress-induced development, sleep, and feeding in invertebrates (Fujiwara et al. 2002, Raizen et al. 2008, You et al. 2008). Its role in appetite control and obesity was first discovered in C. elegans and later in mammals (Valentino et al. 2011). In mammals, a gut peptide, uroguanylin, is released upon feeding and binds to GUCY2C, its receptor in the hypothalamus, to suppress feeding (Valentino et al. 2011). GUCY2C is a membrane guanylyl cyclase (GCY) that produces cGMP upon its activation. Interestingly, there are several previous studies that suggest cGMP functions in obesity. For instance, sildenafil, a medicine that inhibits degradation of cGMP to treat erectile dysfunction, has protective effects in weight gain on a high-fat diet (Ayala et al. 2007, Mitschke et al. 2013). NPs that bind to NP receptors (also GCYs) to produce cGMP are not only important to control blood pressure and heart function (Takei 2001) but also play an important role in lipolysis in adipose tissue via phosphorylation of hormone sensitive lipase by cGMP-dependent protein kinase (PKG) (Sengenes et al. 2000). Furthermore, epidemiological studies show that a certain allele of the NP receptor type C gene is associated with a lean phenotype (Sarzani et al. 2004), suggesting a critical role of NP in fat metabolism.

 

 

[Alex K Chen]

https://pubmed.ncbi.nlm.nih.gov/37910501/

 

[Alex K Chen]

Remember acarbose from here, the drug that effectively turns regular starch into resistant starch? The average and maximum lifespan extension in mice from acarbose may be from the release of a hormone called GLP-17550 from specialized L cells that line our colons.7551 That’s the same hormone mimicked by the expensive new class of injectable weight-loss drugs like Wegovy.7552 This same effect can be obtained in a drug-free manner with prebiotics. Researchers have achieved this in a petri dish7553 or in a person, by infusing their rectum with an SCFA enema7554 or just having them eat fiber7555 or, even better, fiber-rich foods.7556

 

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I don't feel hunger decrease.. but I also tolerate high acarbose very well

[Alex K Chen]

bitter supposedly stimulates GLP-1 through gut receptors, maybe this is also why I seem to become GLP-1 resistant..

Edited November 4 by Alex K Chen