THE MIND Began Hearing In Then?

Tatter Paper of the last blog entrance is not research in the form that any scientist might recognize. Picking the jewel from the walling can get the fingers filthy, but it’s worthwhile. Chance is very helpful sometimes. I happened to notice that also, by chance again, the BMP macros were going to pan out somewhere near 40% fat, using butter as the majority calorie source.

This too is quite fascinating. The post prior to the Tatter Paper post was merely directing out that control C57Bl/6 mice usually do not become obese on their high (40% of calories from fat, chance, nice huh?) fat diet in Ms. Reeves’ PhD. Their weight might be a little heavier on an olive oil-based diet with good PUFA and a little lighter on a stearic acid centered diet with reduced PUFA, but nothing at all dramatic and no weight problems in sight absolutely. Not a perfect match but reasonable. How come this interesting? My (repetitive) idea is that a certain amount of input to the ETC via ETFdh drives reverse electron flow through complex I to limit adipocyte distention.

Stearic acid plus chow starch do this early throughout a meal. Butter plus potato starch does this during a meal early. Canola oil plus potato starch don’t. We’ve no idea whether the butter with potato starch would carry on, long-term, to a slim phenotype in people. The long-term effect of stearate is and of oleate/linoleate is upwards on body weight in mice downwards, but the effect is small. Whoever has read Hyperlipid during the last couple of years will be well aware that I hate advanced signaling.

It usually takes a simple process, like the control of insulin signaling by the proportion of inputs at complicated me, ETFdh, and mtG3Pdh, and sticks a nice, glossy, superficial and opaque surface veneer over it relatively. Then researchers can set off to find 25 or more genes that have some degree of influence at some degree of “higher-ness” of signaling above the core process. We then finish up with a morass of over information with no one linking everything to the primary process. Such a higher-level signaling molecule is leptin. I have got relatively little interest in leptin over the years so may well be lacking large chunks of information which is normal knowledge to others on internet.

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The basic process seems to be that fat’s cells make leptin and the hypothalamus use the info embedded in blood leptin levels to make a lot of decisions about energy homeostasis and energy use. Including hunger. Leptin secretion relates to adipocyte size but deeply underpinning adipocyte size is the ETC’s control of insulin signaling, which models cellular fats content. Leptin seems to provide some long-term modulation of some repeated short-term post-prandial insulin events.

We can remove off the top veneer of longer-term leptin signaling from the primary mitochondrial process by using db/db mice. The db/db mouse has non-functional leptin receptors. This means that the acute effect of mitochondrial signaling within adipocytes is not smoothed over or averaged out by the brain using leptin. The core process in excess fat cells takes over and is seen via body weight and extra fat mass.

At peak energy flux stearic acid generates the utmost level of resistance to insulin’s distending influence on adipocytes. Oleic/linoleic is far less able to generate insulin resistance to limit calorie ingress to each adipocyte. The mice that are db/db homozygous become obese on chow (17% body fat largely PUFA). Within the 40% oleic/linoleic acidity diet they become even more obese because they have a lot of fat molecules to store and a minor ability to withstand insulin’s storage space signaling. Stearic acid given db/db mice also have a ton of fats available for storage. They don’t really lose any weight, however they don’t gain any weight either and they still up pretty damned near to normal mice fed normal chow.

The point of the post is emphasize that excess saturated fat, that I consider to drive physiological adipocyte insulin level of resistance, limits putting on weight in leptin receptor KO mice. The fact it cures their diabetes at the same time is another tale also. I consider that leptin smooths out the distinctions in fat storage made by superoxide signaling from the ETC. I hate this, being truly a great lover of superoxide signaling. Stearate produced superoxide can largely offset the obesogenic effect of being truly a db/db mouse produced by the attendant insufficient leptin signaling. It works together with stearate at 40% of the dietary plan, but not at 17% (elsewhere in the PhD).

Could the butter component of the “tatters” side-step failed leptin signaling (as in obesity) or relative/absolute hypoleptinaemia (as with the post-obese) in the same way a ketogenic diet aspect steps the need for insulin signaling? Could put a human to a high saturated fat ketogenic diet sidestep the majority of the weight problems currently prevalent in the world? A final comment on leptin. I’m unfamiliar with the massive complexity of leptin signaling. It seems to be on and on permanently.