Re: TR : There & Back Again…Lake Reflection, Center Basin, Forester Pass, Milestone Basin – July 26th to Aug. 3rd.
Posted: Thu Aug 11, 2022 2:39 pm
Hi Michael,
I'll second Ian's comments (and your's about him) and add the following summary from a research paper that appeared recently in the journal Nature. It concerns a metabolite that is generated during exercise and suppresses appetite. Obviously, this discovery is going to spur a lot of additional research, but for now, it seems as good an explanation as I've seen for the (counter-intuitive) diminished hunger pangs that I (but not on the same level as you) experience in the Sierra. If you want the full article, let me know and I can attach it to an email. Cameron
Exercise confers protection against obesity, type 2 diabetes and other cardiometabolic diseases1–5. However, the molecular and cellular mechanisms that mediate the metabolic benefits of physical activity remain unclear6. Here we show that exercise stimulates the production of N-lactoyl-phenylalanine (Lac-Phe), a blood-borne signalling metabolite that suppresses feeding and obesity. The biosynthesis of Lac-Phe from lactate and phenylalanine occurs in CNDP2+ cells, including macrophages, monocytes and
other immune and epithelial cells localized to diverse organs. In diet-induced obese mice, pharmacological-mediated increases in Lac-Phe reduces food intake without affecting movement or energy expenditure. Chronic administration of Lac-Phe decreases adiposity and body weight and improves glucose homeostasis. Conversely, genetic ablation of Lac-Phe biosynthesis in mice increases food intake and obesity following exercise training. Last, large activity-inducible increases in circulating Lac-Phe are also observed in humans and racehorses, establishing this metabolite as a molecular effector associated with physical activity across multiple activity modalities and mammalian species. These data define a conserved exercise-inducible metabolite that controls food intake and influences systemic energy balance.
I'll second Ian's comments (and your's about him) and add the following summary from a research paper that appeared recently in the journal Nature. It concerns a metabolite that is generated during exercise and suppresses appetite. Obviously, this discovery is going to spur a lot of additional research, but for now, it seems as good an explanation as I've seen for the (counter-intuitive) diminished hunger pangs that I (but not on the same level as you) experience in the Sierra. If you want the full article, let me know and I can attach it to an email. Cameron
Exercise confers protection against obesity, type 2 diabetes and other cardiometabolic diseases1–5. However, the molecular and cellular mechanisms that mediate the metabolic benefits of physical activity remain unclear6. Here we show that exercise stimulates the production of N-lactoyl-phenylalanine (Lac-Phe), a blood-borne signalling metabolite that suppresses feeding and obesity. The biosynthesis of Lac-Phe from lactate and phenylalanine occurs in CNDP2+ cells, including macrophages, monocytes and
other immune and epithelial cells localized to diverse organs. In diet-induced obese mice, pharmacological-mediated increases in Lac-Phe reduces food intake without affecting movement or energy expenditure. Chronic administration of Lac-Phe decreases adiposity and body weight and improves glucose homeostasis. Conversely, genetic ablation of Lac-Phe biosynthesis in mice increases food intake and obesity following exercise training. Last, large activity-inducible increases in circulating Lac-Phe are also observed in humans and racehorses, establishing this metabolite as a molecular effector associated with physical activity across multiple activity modalities and mammalian species. These data define a conserved exercise-inducible metabolite that controls food intake and influences systemic energy balance.