설탕 갈망 조절, 장내 미생물, 유리 지방산 수용체4, FFAR4

 

 

중국 다롄 화학물리연구소 신먀오량 박사팀은 14일 과학 저널 네이처 미생물학(Nature Microbiology)에서 인간과 생쥐 실험을 통해 장내 박테리아가 식이 설탕 섭취에 대한 선호도 조절과 관련이 있다는 사실을 확인했다고 밝혔다.

동물은 생물학적으로 당분을 좋아하도록 타고나지만, 당분 선호도가 관리되지 않으면 당분 과다 섭취로 인한 고혈당과 대사 질환 위험이 높아질 수 있다.

연구팀은 이전 연구에 따르면 다양한 음식에 대한 갈망은 음식 선호도를 전달하는 핵심 기관인 장에서 뇌로 보내는 신호에서 비롯되는 것으로 보이지만 설탕에 대한 갈망 조절은 복잡하고 장내 미생물의 역할은 불분명하다고 지적했다.


연구팀은 이 연구에서 당뇨병 모델 생쥐 18마리와 제2형 당뇨병 환자 60명의 혈액을 분석하고 이를 건강한 사람 24명의 혈액과 비교했다.

그 결과 당뇨병 쥐와 제2형 당뇨병 환자의 혈액에는 혈당과 식욕을 조절하는 호르몬인 글루카곤 유사 펩티드-1(GLP-1) 분비를 활성화하는 단백질로 긴사슬지방산 수용체인 유리 지방산 수용체4(FFAR4)의 수치가 낮은 것으로 밝혀졌다.

또 당뇨병 쥐는 혈중 FFAR4 수치가 낮을수록 설탕에 대한 선호도가 높아지는 것으로 나타났다.

이와 함께 FFAR4 수치가 낮아지면 장내 미생물인 박테로이데스 불가투스(Bacteroides vulgatus)와 그 대사물질인 판토텐산염(pantothenate) 수치도 감소하는 것으로 밝혀졌다.

또 생쥐 모델에서 판토텐산염은 GLP-1의 분비와 섭식 행동을 조절하는 뇌 영역인 시상하부(hypothalamus)에 직접 작용하는 간 호르몬인 '섬유아세포 성장인자21'(FGF21)의 분비를 담당하는 것으로 나타났다.

연구팀은 당뇨병 생쥐에게 판토텐산염을 먹이거나 장에 박테로이데스 불가투스를 이식하면 설탕을 찾는 행동이 현저히 감소한다는 사실을 확인했다.

이는 설탕에 대한 갈망 조절에 장내 미생물이 관여하는 장-간-두뇌 연결 메커니즘이 중요한 역할을 한다는 것을 시사한다고 연구팀은 설명했다.

연구팀은 이 연구 결과는 설탕 선호를 억제하는 데 FFAR4가 중요하다는 사실을 보여준다며 장내 미생물 박테로이데스 불가투스와 그 대사물질 판토텐산염이 당뇨병의 잠재적인 치료 표적이 될 수 있을 것이라고 말했다.

 

 

In the scientific journal Nature Microbiology on the 14th, Dr. Shin Maoliang's team at the Dalian Institute of Chemical Physics in China confirmed that intestinal bacteria are related to controlling preferences for dietary sugar intake through human and mouse experiments.

Animals are biologically born to like sugar, but if sugar preferences are not managed, the risk of hyperglycemia and metabolic disease due to excessive sugar consumption can be increased.

The team pointed out that previous studies have shown that cravings for various foods appear to come from signals sent from the intestine to the brain, a key organ that transmits food preferences, but the control of cravings for sugar is complex and the role of intestinal microbes is unclear.


The research team analyzed the blood of 18 diabetes model mice and 60 type 2 diabetes patients in the study and compared them with the blood of 24 healthy people.

As a result, it was found that the blood of diabetic mice and type 2 diabetes patients had low levels of free fatty acid receptor 4, a long-chain fatty acid receptor, as a protein that activates the secretion of glucagon-like peptide-1 (GLP-1), a hormone that controls blood sugar and appetite.

In addition, diabetic mice have a higher preference for sugar as their blood FFAR4 levels are lower.

In addition, lower FFAR4 levels have also been found to reduce the levels of Bacteroides bulgatus, an intestinal microorganism, and pantothenate, a metabolite.

In addition, in mouse models, pantothenate was found to be responsible for the secretion of "fibroblast growth factor 21" (FGF21), a liver hormone that directly acts on the hypothalamus, a brain region that controls the secretion and feeding behavior of GLP-1.

The research team confirmed that feeding pantothenate to diabetic mice or implanting Bacteroides vulgatus into their intestines significantly reduced sugar-seeking behavior.

This suggests that the intestinal-liver-brain connection mechanism, in which intestinal microbes are involved in the regulation of sugar cravings, plays an important role, the research team explained.

The research team said the findings show that FFAR4 is important in suppressing sugar preference, and that intestinal microorganisms Bacteroides vulgatus and its metabolite pantothenate could be potential therapeutic targets for diabetes.