반 글루타이드혈당 수치를 낮추고 인슐린 분비를 향상시키는 것으로 알려진 펩티드 인 자연 발생 GLP-1의 유도체입니다. 연구에 따르면 세 마 글루 타이드는 심장, 간 및 폐 기능을 개선하면서 알츠하이머 병의 효과를 늦추거나 예방할 수 있습니다. semaglutide는 위 배출을 지연시키고 장 운동성을 감소시킴으로써 식욕을 크게 감소시키는 것으로 나타났습니다. 글루카곤-유사 펩티드 -1 (GLP-1) 아날로그는 인슐린을 자극하고 포도당 의존적 방식으로 글루카곤 분비를 억제하는 것으로 나타났다.
유리 (1) 30 ml 세균성 물
자격을 갖춘 주문이 있습니다$ 500 USD.
(캡슐 제품, 미용 펩티드, 프로모션 코드 및 배송 제외)
반 글루타이드혈당 수치를 낮추고 인슐린 분비를 향상시키는 것으로 알려진 펩티드 인 자연 발생 GLP-1의 유도체입니다. 연구에 따르면 세 마 글루 타이드는 심장, 간 및 폐 기능을 개선하면서 알츠하이머 병의 효과를 늦추거나 예방할 수 있습니다. semaglutide는 위 배출을 지연시키고 장 운동성을 감소시킴으로써 식욕을 크게 감소시키는 것으로 나타났습니다. 글루카곤-유사 펩티드 -1 (GLP-1) 아날로그는 인슐린을 자극하고 포도당 의존적 방식으로 글루카곤 분비를 억제하는 것으로 나타났다.
제품 사용 :이 제품은 연구 화학 물질로만 의도 된 것입니다.이 명칭은 시험 관내 시험 및 실험실 실험에만 연구 화학 물질을 엄격하게 사용할 수있게한다. 이 웹 사이트에서 제공되는 모든 제품 정보는 교육 목적으로 만 사용됩니다. 인간이나 동물에 어떤 종류의 신체적으로 소개되는 것은 법에 의해 엄격히 금지되어 있습니다. 이 제품은 라이센스가 부여 된 자격을 갖춘 전문가 만 처리해야합니다. 이 제품은 약물, 음식 또는 화장품이 아니며 약물, 음식 또는 화장품으로 잘못 브랜드화되거나 잘못 사용되거나 오해가되지 않을 수 있습니다.
글루카곤과 유사한 펩티드 -1의 짧은 짧은 GLP-1은 길이가 30-31 아미노산에 불과한 짧고 자연적으로 발생하는 펩티드 호르몬이다. 주요 생리 학적 기능은 자연적으로 인슐린 분비를 향상시켜 혈당 수치를 낮추는 것입니다. 또한 인슐린 유전자 전사를 촉진하여 보호 베타 세포 인슐린 저장에서 역할을하며 뇌 및 중추 신경계에서의 신경 영양 효과와 관련이 있습니다. GI 시스템에서, GLP-1은 위 배출을 지연시키고 장 운동성을 감소시킴으로써 식욕을 크게 감소시키는 것으로 나타났다. 예비 연구는 심장, 지방, 근육, 뼈, 간, 폐 및 신장에서도 GLP-1의 영향을 보여주었습니다.
GLP-1 연구의 주요 초점은 식욕 억제뿐만 아니라 당뇨병 치료/예방 영역에있었습니다. 2 차 연구는 펩티드의 잠재적 심혈관 이점에 중점을 둡니다. 보다 최근의 연구는 덜 강력한 연구는 신경 퇴행성 질환을 막는 GLP-1의 능력에 중점을 둡니다. 이 후자의 연구 영역은 최신이지만, 펩티드가 알츠하이머 병의 설정에서 아밀로이드 베타 플라크의 축적을 느리게하거나 방지하는 것으로 밝혀졌다.
순서: hxegtftsdvssylegqaak-oh.teric diacid-efiawlvrgrg
분자식: C187H291N45O59
분자량: 4113.64g/mol
Pubchem Cid: 56843331
CAS 번호: 910463-68-2
동의어: Semaglutide, Oxempic, Rybelsus, NN9535
Holst 박사에 따르면 GLP-1이 가진 가장 중요한 효과는 아마도 "incretin 효과"라고합니다. 인크 레틴은 혈액 포도당 (당) 수준이 감소하는 GI Tract에 의해 방출되는 대사 호르몬 그룹입니다. GLP-1은 설치류 모델에서 인크 레틴 효과를 자극하는 두 가지 가장 중요한 호르몬 (GIP) 중 하나 인 것으로 나타났습니다. GIP는 GLP-1의 수준보다 약 10 배 높은 수준에서 순환하지만, 특히 혈당 수준이 상당히 높을 때 GLP-1이 두 분자 중 더 강력하다는 증거가 있습니다.
A GLP-1 receptor has been identified on the surface of pancreatic beta cells, making it clear that GLP-1 directly stimulates the exocytosis of insulin from the pancreas. When combined with sulfonylurea drugs, GLP-1 has been shown to boost insulin secretion enough to cause mild hypoglycemia in up to 40% of subjects[1]. Of course, increased insulin secretion is associated with a number of trophic effects including increased protein synthesis, reduction in the breakdown of protein, and increased uptake of amino acids by skeletal muscle.
Research in animal models suggests that GLP-1 can stimulate the growth and proliferation of pancreatic beta cells and that it may stimulate the differentiation of new beta cells form progenitors in the pancreatic duct epithelium. Research has also shown that GLP-1 inhibits beta cell apoptosis[1]. Taken in sum, these effects tip the usual balance of beta cell growth and death toward growth, suggesting that the peptide may be useful in treating diabetes and in protecting the pancreas against insult that harms beta cells.
In one particularly compelling trial, GLP-1 was shown to inhibit the death of beta cells caused by enhanced levels of inflammatory cytokines. In fact, mouse models of type 1 diabetes have revealed that GLP-1 protects islet cells from destruction and may, in fact, be a useful means of preventing onset of the type 1 diabetes[2].
Research in mouse models suggests that administration of GLP-1, and its similar cousin GLP-1, into the brains of mice can reduce the drive to eat and inhibit food intake[3]. It appears that GLP-1 may actually enhance feelings of satiety, helping individuals to feel fuller and reducing hunger indirectly. Recent clinical studies have shown in mice that twice daily administration of GLP-1 receptor agonists cause gradual, linear weight loss. Over a long period, this weight loss is associated with significant improvement in cardiovascular risk factors and a reduction in hemoglobin A1C levels, the latter of these being a proxy marker for the severity of diabetes and the quality of blood sugar control attained via treatment[4].
It is now know that GLP-1 receptors are distributed throughout the heart and act to improve cardiac function in certain settings by boosting heart rate and reducing left ventricular end-diastolic pressure[5]. The latter may not seem like much, but increased LV end-diastolic pressure is associated with LV hypertrophy, cardiac remodeling, and eventual heart failure.
Recent evidence has even suggested that GLP-1 could play role in decreasing the overall damaged caused by a heart attack. It appears that the peptide improves cardiac muscle glucose uptake, thereby helping struggling ischemic heart muscle cells to get the nutrition they need to continue functioning and avoid programmed cell death. The increase in glucose uptake in these cells appears to independent of insulin[6].
Large infusions of GLP-1 into dogs have been shown to improve LV performance and reduce systemic vascular resistance. The latter effect can help to reduce blood pressure and ease strain on the heart as a result[7]. This, in turn, can help to reduce the long-term consequences of high blood pressure such as LV remodeling, vascular thickening, and heart failure. According to Dr. Holst, administration of GLP-1 following cardiac injury has “constantly increased myocardial performance both in experimental animal models and in patients.”
There is some evidence to suggest that GLP-1 can improve learning and help to protect neurons against neurodegenerative diseases such as Alzheimer’s disease. In one study, GLP-1 was shown to enhance associative and spatial learning in mice and even to improve learning deficits in mice with specific gene defects. In rats that over-express the GLP-1 receptor in certain regions of the brain, learning and memory are both significantly better than in their normal controls[8].
Additional research in mice has shown that GLP-1 can help to protect against excitotoxic neuron damage, completely protecting rat models of neurodegeneration against glutamate-induced apoptosis. The peptide can even stimulate neurite outgrowth in cultured cells. Researchers are hopeful that additional research on GLP-1 will reveal how it might be used to halt or reverse certain neurodegenerative diseases[9].
Interestingly, GLP-1 and its analogue exendin-4 have been shown in mouse models to reduce levels of amyloid-beta in the brain as well as the beta-amyloid precursor protein found in neurons. Amyloid beta is the primary component of the plaques observed in Alzheimer’s disease, plaques which, while not necessarily known to be causative, are associated with the severity of the disease. It remains to be seen if preventing amyloid beta accumulation can protect against the effects of Alzheimer’s disease, but this research is, at the very least, a tantalizing clue as to how scientists my intervene in the progression of mild cognitive impairment to full Alzheimer’s disease[10].
GLP-1 exhibits minimal to moderate side effects, low oral and excellent subcutaneous bioavailability in mice. Per kg dosage in mice does not scale to humans. GLP-1 for sale at
The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.
In 1986 Professor Jens Juul Holst discovered the GLP-1 hormone in connection with his work on stomach ulcer surgery. Since the discovery, Novo Nordisk have used the research to successfully develop products to treat diabetes and obesity. The hormone GLP-1 can be used to regulate blood sugar levels and satiety. Not only has it made treatment of obesity and diabetes possible, it has also proven useful preventatively through early diagnosis for citizens who are at risk of developing diabetes and obesity. In 2015, Jens Juul Holst received the prestigious international Fernström prize for his research on GLP-1. He is one of the most cited researchers in Europe, with over 1,200 published articles and citations in over 3,500 articles annually.
Professor Jens Juul Holst is being referenced as one of the leading scientists involved in the research and development of GLP-1. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between
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