GLP-1, kort voor glucagon-achtige peptide-1 is een kort, natuurlijk voorkomend peptidehormoon slechts 30-31 aminozuren lang. De primaire fysiologische functie is om de bloedsuikerspiegel te verlagen door de insulinesecretie op natuurlijke wijze te verbeteren. Het speelt ook rollen in de insulinevoorraden van de bescherming van de bescherming door insuline -gentranscriptie te bevorderen en is gekoppeld aan neurotrofe effecten in de hersenen en het centrale zenuwstelsel. In het GI-systeem is aangetoond dat GLP-1 de eetlust aanzienlijk vermindert door maaglediging te vertragen en de darmmotiliteit te verminderen. Voorlopig onderzoek heeft ook gevolgen aangetoond van GLP-1 in het hart, vet, spieren, botten, lever, longen en nieren.

De primaire focus van GLP-1-onderzoek is op het gebied van diabetesbehandeling/preventie en eetlustonderdrukking. Secundair onderzoek richt zich op de potentiële cardiovasculaire voordelen van het peptide. Recenter, en dus minder robuust, richt onderzoek zich op het vermogen van GLP-1 om neurodegeneratieve ziekte te voorkomen. Hoewel dit laatste onderzoeksgebied nieuwste is, is het ook het snelgroeiende gebied van GLP-1-onderzoek nu is dat het peptide is aangetoond dat het de accumulatie van amyloïde bèta-plaques in de setting van de ziekte van Alzheimer vertraagt ​​of voorkomen.

Bron:Pubch

Reeks: HXEGTFTSDVSSYLEGQAAK-OH.STERIC DIACID-EFIAWLVRGRG
Moleculaire formule: C187H291N45O59
Molecuulgewicht: 4113.64g/mol
Pubchem cid: 56843331
CAS -nummer: 910463-68-2
Synoniemen: Semaglutide, Oxempic, Rybelsus, NN9535

Het incretine-effect van GLP-1

Misschien wel het belangrijkste effect dat GLP-1 heeft, volgens Dr. Holst, wordt het 'incretine-effect' genoemd. Incretines zijn een groep metabole hormonen, vrijgegeven door het maagdarmkanaal, die een afname van bloedglucose (suiker) niveaus veroorzaken. Van GLP-1 is aangetoond dat het een van de twee belangrijkste hormonen (de andere is GIP) is om het incretine-effect in knaagdiermodellen te stimuleren. Hoewel GIP circuleert op niveaus die ongeveer 10 keer hoger zijn dan die van GLP-1, zijn er aanwijzingen dat GLP-1 de krachtiger is van de twee moleculen, vooral wanneer niveaus van bloedglucose vrij hoog zijn.

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.

GLP-1 and Beta Cell Protection

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].

GLP-1 and Appetite

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].

Potential Cardiovascular Benefits of GLP-1

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.”

GLP-1 and the Brain

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

1. “The Physiology of Glucagon-like Peptide 1 | Physiological Reviews.” [Online].
2. “Combined treatment with lisofylline and exendin-4 reverses autoimmune diabetes. – PubMed – NCBI.” [Online].
3. “The proglucagon-derived peptide, glucagon-like peptide-2, is a neurotransmitter involved in the regulation of food intake. – PubMed – NCBI.” [Online].
4. “Interim analysis of the effects of exenatide treatment on A1C, weight and cardiovascular risk factors over 82 weeks in 314 overweight patients with… – PubMed – NCBI.” [Online].
5. “Cardiac function in mice lacking the glucagon-like peptide-1 receptor. – PubMed – NCBI.” [Online].
6. “Glucagon-like Peptide 1 Can Directly Protect the Heart Against Ischemia/Reperfusion Injury | Diabetes.” [Online].
7. “Recombinant glucagon-like peptide-1 increases myocardial glucose uptake and improves left ventricular performance in conscious dogs with pacing-ind… – PubMed – NCBI.” [Online].
8. “Glucagon-like peptide-1 receptor is involved in learning and neuroprotection. – PubMed – NCBI.” [Online].
9. “Protection and reversal of excitotoxic neuronal damage by glucagon-like peptide-1 and exendin-4. – PubMed – NCBI.” [Online].
10. “A new Alzheimer’s disease interventive strategy: GLP-1. – PubMed – NCBI.” [Online].
11. Holst JJ. From the Incretin Concept and the Discovery of GLP-1 to Today’s Diabetes Therapy. Front Endocrinol (Lausanne). 2019;10:260. Published 2019 Apr 26. doi:10.3389/fendo.2019.00260 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6497767/

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