Японы Осакагийн их сургуулийн судлаачид тархины тодорхой уураг нь өөх тостой хоол хүнс сонгох болон жин нэмэх үйл явцад хэрхэн нөлөөлдөг болохыг илрүүлжээ.
FASEB Journal сэтгүүлд нийтлэгдсэн уг судалгаагаар “optic atrophy-1” (OPA1) хэмээх уураг нь эсийн эрчим хүчний эх үүсвэр болох митохондрийн үйл ажиллагаанд чухал үүрэгтэй болохыг тогтоосон байна. Судлаачид хулганы загвар ашиглан MC4R рецептор агуулсан мэдрэлийн эсүүд дэх OPA1 уургийн үүргийг судалжээ. Тархины гипоталамус бүсэд байрлах эдгээр эс нь бодисын солилцоо, өлсгөлөн болон цатгалан байдлыг зохицуулдаг байна.
Туршилтаар OPA1 уураг дутагдалтай хулганууд өөх тос ихтэй хоол хүнсийг илүүд үзэж, илүү хурдан жин нэмж байсныг илрүүлжээ. Энэхүү нөлөө нь эмэгчин хулгануудад илүү тод ажиглагдсан байна. Мөн OPA1 уургийн дутагдал нь хоолны дуршлыг дарах эмчилгээний үр дүнд сөргөөр нөлөөлж буйг судлаачид тэмдэглэжээ.
Судлаач Шигенобу Мацумурагийн хэлснээр, энэхүү олдвор нь таргалалтын механизмыг мэдрэлийн эсийн эрчим хүчний солилцооны үүднээс ойлгоход чухал ач холбогдолтой юм. Хэдийгээр энэ нь амьтны загвар дээр хийсэн судалгаа боловч, ирээдүйд хүний таргалалтыг эмчлэх хувийн тохиргоотой эмчилгээний арга боловсруулахад суурь судалгаа болж магадгүй байна.
Дэлгэрэнгүйг эх сурвалжаас харах
↓Эх сурвалжийг нээх ↓
With health problems related to poor diets and obesity continuing to become more widespread, researchers are hunting for the specific biological mechanisms behind preferences for fatty foods – and for potential ways to dial them down.
If we uncover the brain cells and pathways responsible for increasing the likelihood of eating too much or preferring unhealthy types of food (even when we know they’re bad for us), then it follows that we might be able to nudge them back in the right direction too.
Now researchers led by a team from Osaka Metropolitan University in Japan have found that one neural protein in particular can have a significant effect on fat intake and weight gain in mice.
The study, published in the FASEB Journal, identifies optic atrophy-1 (OPA1) as well worth investigating further. The protein is responsible for the smooth running of cell batteries known as mitochondria, and when it’s absent, eating patterns change.
“Our findings provide key insights into the mechanisms underlying obesity from the perspective of neuronal energy metabolism,” says nutritionist Shigenobu Matsumura, from Osaka Metropolitan University.
The researchers wanted to follow up on previous studies linking missing OPA1 with obesity in animals, and this time focused on OPA1 inside appetite-related neurons carrying the melanocortin 4 receptor (MC4R) protein.
MC4R-carrying neurons play a crucial role in the hypothalamus brain region, which in turn is largely responsible for energy management (metabolism) in the body, and appetite and hunger. These neurons tell us when it’s time to eat, and when it’s time to burn energy.
Mice engineered to lack the OPA1 protein in MC4R neurons were found to have a significantly higher preference for dietary fat, compared to control mice, and gained weight quicker – with the effects more pronounced in females versus males.
Over time, these mice developed obesity, though this took several weeks to emerge. The suggestion is that OPA1 might become more important as we get older – bearing in mind that mice live for months rather than years.
“This study provides new insight into how mitochondrial function in the hypothalamus is linked to energy metabolism under conditions of dietary fat intake,” write the researchers.
Overall, the study is solid evidence that missing or impaired OPA1 proteins cause these appetite-controlling neurons to be less effective, due to the reduction in mitochondria-supplied energy that OPA1 helps ensure.
The findings do have their nuances though: The researchers demonstrated that a lack of OPA1 didn’t break the MC4R messaging completely, by reactivating it with an anti-obesity drug.
Interestingly, the drug worked as expected in males regardless of OPA1 status. But in females, losing OPA1 blunted the drug’s ability to suppress food intake – hinting that the sex differences seen throughout the study extend even to how mice respond to treatment.
“Pharmacological activation of MC4R suppressed food intake under baseline-matched conditions, indicating that MC4R signaling is not abolished,” write the researchers.
Of course this is a study exclusively in mouse models, so it’s not guaranteed that the same processes and pathways are involved in the human brain – even if decades of scientific study using mice as human substitutes suggests that it’s likely.
If these findings can be replicated in people, then it ties in directly to the decisions we make when shopping for groceries or choosing where to eat out. In certain cases, unhealthy choices, and the consequences of them, might be partly down to that OPA1 protein and whether it’s working at capacity.
We know that obesity is a significant public health problem, which increases the risk of further complications related to heart disease, diabetes, osteoarthritis, and more.
Related: Obesity Is a Form of Premature Aging, Scientists Say, And We Need to Rethink It
Further down the line, finding ways to deal with the tiny power failures in these specific neurons could be another way forward for treatments tackling over-eating and obesity – though clearly these are issues involving many overlapping factors and triggers.
“The sex differences observed in OPA1 responses and obesity susceptibility may help inform the development of obesity treatments that take them into account, as well as future personalized medicine approaches,” says Matsumura.
The research has been published in the FASEB Journal.
This article was fact-checked by Fiona MacDonald and edited by Fiona MacDonald. While we pride ourselves on our process, we are only human. If you spot a mistake, please let us know.
