{"id":112207,"date":"2024-07-12T14:55:33","date_gmt":"2024-07-12T14:55:33","guid":{"rendered":"https:\/\/rochellesthrezrs.com\/how-signal-molecule-versions-impact-weight-loss\/"},"modified":"2024-07-12T14:55:33","modified_gmt":"2024-07-12T14:55:33","slug":"how-signal-molecule-versions-impact-weight-loss","status":"publish","type":"post","link":"https:\/\/rochellesthrezrs.com\/how-signal-molecule-versions-impact-weight-loss\/","title":{"rendered":"How Signal Molecule Versions Impact Weight Loss"},"content":{"rendered":"


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Researchers have discovered why some individuals lose weight more slowly than others post-workout. Their study focused on mice unable to produce signal molecules crucial for responding to short-term exercise and regulating energy metabolism. These mice showed reduced oxygen consumption during exercise, burned less fat, and were more prone to weight gain. () <\/p>\n

It is well known that exercise leads to the burning of fat. But for some people, this is much more difficult than for others, casting doubt on whether the mechanism behind losing or gaining weight is as simple as \u201ccalories in minus calories out.\u201d <\/p>\n

\u2018Appetite-suppressing #antiobesity drugs have emerged, gaining popularity globally. Yet, there remains a lack of drugs that address #obesity by increasing energy expenditure. #appetite \u2019
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Exploring Variants of the Signal Molecule PGC-1\u237a: Insights into Exercise Effects<\/h2>\n

Researchers have previously identified a signal molecule, a protein by the name of \u201cPGC-1\u237a,\u201d that seems to link exercise and its effects. However, whether an increased amount of this protein actually leads to these effects or not has been inconclusive, since some experiments suggested it while others didn\u2019t. More recently, the Kobe University endocrinologist OGAWA Wataru as well as other researchers found that there are actually a few different versions of this protein. <\/p>\n

Ogawa explains: \u201cThese new PGC-1\u03b1 versions, called \u201cb\u201d and \u201cc,\u201d have almost the same function as the conventional \u201ca\u201d version, but they are produced in muscles more than tenfold more during exercise, while the a version does not show such an increase.\u201d His team therefore set out to prove the idea that it is the newly discovered versions, and not the previously known one, that regulate the energy metabolism during workouts. <\/p>\n

To do so, the researchers created mice that lack the b and c versions of the signal molecule PGC-1\u237a while they still have the standard a version, and measured the mice\u2019s muscle growth, fat burning and oxygen consumption during rest and short-term as well as long-term workout. They also recruited human test subjects with and without type 2 diabetes and submitted them to similar tests as the mice, because insulin-intolerant and obese people are known to have reduced levels of the signal molecule. <\/p>\n

Ogawa and his team published their results in the journal Molecular Metabolism.<\/i> They found that, while all versions of the signal molecule cause similar biological reactions, their different levels of production have far-reaching consequences for the organism\u2019s health. The lack of the alternative b and c versions of PGC-1\u237a means that the organism is essentially blind to short-term activity and does not adapt to these stimuli, with the effect that such individuals consume less oxygen and burn less fat during and after workouts. <\/p>\n

In humans, the research team found that the more the test subjects produced the b and c versions of the signal molecule, the more they consumed oxygen and the less percent body fat they had, across healthy individuals and those with type 2 diabetes. \u201cThus, the hypothesis that the genes in skeletal muscle determine susceptibility to obesity was correct,\u201d summarizes Ogawa these findings. However, they also found that long-term exercise stimulates the production of the standard a version of PGC-1\u237a, and mice that exercised regularly over the course of six weeks exhibited an increase in muscle mass irrespective of whether they could produce the alternative versions of the signal molecule or not. <\/p>\n

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In addition to the production in muscles, the Kobe University team looked at how the production of the different versions of PGC-1\u237a changes in fat tissues, and found no relevant effect in response to exercise. However, since animals also burn fat to maintain body temperature, the researchers also investigated the mice\u2019s ability to tolerate cold. <\/p>\n

And indeed, they found that the production of the b and c versions of the signal molecule in brown adipose tissue is increased when the animals are exposed to cold, and that the body temperature of individuals that cannot produce these versions dropped significantly under these conditions. On the one hand, this may contribute to these individuals\u2019 having more body fat, but on the other hand it seems to imply that the b and c versions of the signal molecule may be responsible for metabolic adaptations to short-term stimuli more generally. <\/p>\n

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Ogawa and his team point out that understanding the physiological activity of the different versions of PGC-1\u237a might allow to devise treatment approaches for obesity: \u201cIf a substance that increases the b and c versions can be found, this could lead to the development of drugs that enhance energy expenditure during exercise or even without exercise. Such drugs could potentially treat obesity independently of dietary restrictions.\u201d The team are now conducting research to find out more about the mechanisms that lead to the increased production of the signal molecule\u2019s b and c versions during exercise. <\/p>\n

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  1. Adaptive gene expression of alternative splicing variants of PGC-1\u237a regulates whole-body energy metabolism – (https:\/\/linkinghub.elsevier.com\/retrieve\/pii\/S2212877824000991)<\/span><\/li>\n<\/ol>\n

    Source-Eurekalert<\/p><\/div>\n