Pancragen is een natuurlijk voorkomende tetrapeptide -bioregulator die, zoals de naam al aangeeft, primaire effecten heeft op de alvleesklier. Niet te verwarren met de op DNA gebaseerde pancragentest, is aangetoond dat pancrageen de bloedsuikerspiegel helpt bij het beheersen, de endocriene functie van de pancreas verbeteren, melatonine-expressie reguleren en de incidentie en omvang van het metabool syndroom vermindert. Het is onderzocht en is interessant voor de behandeling van zowel diabetes als de metabole effecten van veroudering. Tot op zekere hoogte kan pancragen worden beschouwd als een anti-verouderingspeptide voor de alvleesklier.

Amino Acid Sequence: Lys-Glu-Asp-Trp (KEDW) Molecular Formula: C₂₆H₃₆N₆O₉ Molecular Weight: 576.25 g/mol PubChem CID: 68452887 Synonyms: SCHEMBL5491754 Source: PepDraw

Onderzoek naar pancreascellen toont aan dat pancragen de expressie stimuleert van een aantal differentiatiefactoren die de groei van acinaire en eilandje van Langerhans -cellen regelen. De laatste zijn verantwoordelijk voor insuline en glucagon [1]. Hoewel dit misschien geen anti-verouderingseffect lijkt, moet het duidelijk zijn dat herstel van verbeterde groei en differentiatie een kenmerk is van jonge, gezonde weefsels. Het verbeteren van deze parameters, met name in oudere weefsels, is fundamenteel een anti-verouderingseffect. Gedurende de rest van de secties van Pancragen zullen aanvullende redenen voor de classificatie ervan als een anti-verouderingspeptide duidelijk zijn. In het bijzonder is het vermogen om de epigenetische regulatie van DNA te veranderen om de genexpressie te verbeteren een van de duidelijkste indicaties dat pancragen de klok op DNA kan terugdraaien om de functie meer te bevorderen in overeenstemming met de jeugd.

Pancragen en metabole stoornissen

Further supporting the idea that Pancragen is an anti-aging peptide are its effects on metabolic disorders. Research shows that metabolic dysregulation in older people is at least partially caused by changes in melatonin secretion during sleep. This melatonin deficiency appears to be caused by changes in insulin levels, suggesting that loss of insulin function, both in disease and as a result of old age, may be responsible for changes in melatonin secretion, which is then responsible for some of the other symptoms of metabolic syndrome[2]. Based on the above line of thought, it stands to reason that administration of Pancragen, which helps to normalize insulin secretion, could further reduce symptoms of metabolic syndrome by normalizing melatonin secretion. In fact, this is precisely what research reveals. Administration of Pancragen decreases glucose levels but also reduces plasma concentrations of insulin as well as the insulin resistance index which are strong indications that Pancragen is having a direct effect on melatonin signaling[2]. Both exogenous and endogenous melatonin inhibit the pathophysiological mechanisms of metabolic syndrome and normalize metabolism[3]. Research shows that melatonin receptors exist in the pancrease where they serve to modulate insulin and glucagon signaling in a diurnal (daylight-sensitive) fashion[4]. There is a lot of new research focusing on how disruptions in melatonin signaling are linked to the development of type 2 diabetes and metabolic syndrome. If melatonin affects the pancreas, then is stands to reason that there is likely a feedback mechanism by which glucagon and insulin signal to the pineal gland whether to increase or decrease melatonin release. In fact, this feedback loop exists and, in type 2 diabetes, appears to be responsible for the additional metabolic effects that arise in this version of the disease that are less common in type 1 diabetes. This would explain why Pancragen’s ability to regulate insulin secretion of the pancreas also has beneficial effects on other symptoms of metabolic syndrome. Source: Pubch

Pancragen en diabetes

Of course, the most obvious use for Pancragen is in the treatment of diabetes, hyperinsulinemia, and elevated blood glucose levels. Research in rhesus monkeys comparing Pancragen to glimepiride (a widely used drug for lowering blood sugar) reveals that while both compounds can reduce blood sugar levels to normal baselines, only Pancragen normalizes insulin levels and C-peptide levels[5], [6]. This would suggest that Pancragen is having a more physiologic effect, striking at the very heart of what causes elevated blood sugar and correcting the problem at a more fundamental level. Research in old monkeys shows that Pancragen normalizes plasma insulin, C-peptide, and glucose levels within 10 days and that the effect lasts, at least partially, for as long as 3 weeks[7], [8]. This suggests that Pancragen might be useful in restoring pancreatic function in elderly individuals or maintaining it as we age. This can help to normalize the metabolic system and reduce the impact of everything from osteoporosis to dementia. Additional research in cell cultures shows that Pancragen increases the expression of matrix metalloproteinases MMP2 and MMP9. It also increases the expression of serotonin, glycoprotein CD79alpha, and the anti-apoptotic protein MCl1 while decreasing levels of the pro-apoptotic protein p53. Additionally, levels of proliferation markers PCNA and Ki67 are increased. Vasili Ashapkin, author of the textbook DNA -methylatie in planten and collaborator with Vladimir Khavinson, points out that these findings collectively indicate that Pancragen activates the expression of signaling molecules associated with increased differentiation and functionality of pancreatic islet cells[9], [10]. These effects can only be accounted for by a broad functional mechanism such as direct alteration of DNA expression and condensation patterns. In other words, Pancragen is likely working at a very fundamental level within the DNA to alter the expression of multiple genes.

Pancragen en het vasculaire systeem

One of the most serious consequences of diabetes is on the function of small blood vessels called capillaries. Elevated glucose levels cause these capillaries to first become leak and then to die off as the cells that make them up, called endothelial cells, become dysfunctional and then die. Many of the long-term consequences of diabetes like heart disease, kidney disease, erectile dysfunction, and loss of limb result from damage to and loss of capillaries. Research on Pancragen shows that it helps to normalize the adhesion of mesenteric capillary endothelium[11]. These findings suggest that Pancragen could protect the endothelium from some of the effects of diabetes, thus helping to stave off long-term consequences of the disease.

Pancragen en het vasculaire systeem

Een van de ernstigste gevolgen van diabetes is op de functie van kleine bloedvaten die haarvaten worden genoemd. Verhoogde glucosewaarden zorgen ervoor dat deze haarvaten eerst lekken en vervolgens afsterven terwijl de cellen die ze verzinnen, endotheelcellen worden genoemd, disfunctioneel worden en vervolgens sterven. Veel van de langdurige gevolgen van diabetes zoals hartaandoeningen, nierziekte, erectiestoornissen en verlies van ledematen zijn het gevolg van schade aan en verlies van haarvaten.

The above literature was researched, edited and organized by Dr. E. Logan, M.D. Dr. E. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.

Vladimir Khavinson is a Professor, President of the European region of the International Association of Gerontology and Geriatrics; Member of the Russische en Oekraïense academies van medische wetenschappen; Main gerontologist of the Health Committee of the Government of Saint Petersburg, Russia; Director of the Saint Petersburg Institute of Bioregulation and Gerontology; Vice-president of Gerontological Society of the Russische Academie van Wetenschappen; Head of the Chair of Gerontology and Geriatrics of the North-Western State Medical University, St-Petersburg; Colonel of medical service (USSR, Russia), retired. Vladimir Khavinson is known for the discovery, experimental and clinical studies of new classes of peptide bioregulators as well as for the development of bioregulating peptide therapy. He is engaged in studying of the role of peptides in regulation of the mechanisms of ageing. His main field of actions is design, pre-clinical and clinical studies of new peptide geroprotectoren. A 40-year-long investigation resulted in a multitude of methods of application of peptide bioregulators to slow down the process of ageing and increase human life span. Six peptide-based pharmaceuticals and 64 peptide food supplements have been introduced into clinical practice by V. Khavinson. He is an author of 196 patents (Russian and international) as well as of 775 scientific publications. His major achievements are presented in two books: “Peptides and Ageing” (NEL, 2002) and “Gerontological aspects of genome peptide regulation” (Karger AG, 2005). Vladimir Khavinson introduced scientific specialty “Gerontology and Geriatrics” in the Russian Federation on the governmental level. Academic Council headed by V. Khavinson has oversighted over 200 Ph.D. and Doctorate theses from many different countries. Prof. Vladimir Khavinson is being referenced as one of the leading scientists involved in the research and development of Pancragen. 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. V. K. Khavinson et al., “Effects of pancragen on the differentiation of pancreatic cells during their ageing,” Bull. Exp. Biol. Med., Vol. 154, nee. 4, pp. 501–504, februari 2013, doi: 10.1007/s10517-013-1987-6.
2. O. V. Korkushko, V. K. Khavinson, V. B. Shatilo, I. A. Antonyk-Sheglova, and E. V. Bondarenko, “Prospects of using pancragen for correction of metabolic disorders in elderly people,” Bull. Exp. Biol. Med., Vol. 151, nee. 4, pp. 454–456, augustus 2011, doi: 10.1007/s10517-011-1354-4.
3. S. I. Rapoport, A. I. Molchanov, V. A. Golichenkov, O. V. Burlakova, E. S. Suprunenko, and E. S. Savchenko, “[Metabolic syndrome and melatonin],” Klin. Med. (Mosk.), Vol. 91, nee. 11, pp. 8–14, 2013.
4. E. Peschke, I. Bähr, and E. Mühlbauer, “Melatonin and pancreatic islets: interrelationships between melatonin, insulin and glucagon,” Int. J. Mol. Sci., Vol. 14, nee. 4, pp. 6981–7015, maart 2013, doi: 10.3390/ijms14046981.
5. N. D. Goncharova, L. G. Ivanova, T. E. Oganyan, A. A. Vengerin, and V. K. Khavinson, “[Correction of impaired glucose tolerance using tetrapeptide (Pancragen) in old female rhesus monkeys],” Adv. Gerontol. Uspekhi Gerontol., Vol. 28, nee. 3, pp. 579–585, 2015.
6. V. K. Khavinson, M. M.-G. Gapparov, N. E. Sharanova, A. V. Vasilyev, and G. A. Ryzhak, “Study of biological activity of Lys-Glu-Asp-Trp-NH2 endogenous tetrapeptide,” Bull. Exp. Biol. Med., Vol. 149, nee. 3, pp. 351–353, september 2010, doi: 10.1007/s10517-010-0944-x.
7. N. D. Goncharova, L. G. Ivanova, T. É. Oganian, A. A. Vengerin, and V. K. Khavinson, “[Impact of tetrapeptide pancragen on endocrine function of the pancreas in old monkeys],” Adv. Gerontol. Uspekhi Gerontol., Vol. 27, nee. 4, pp. 662–667, 2014.
8. I. M. Kvetnoi, A. P. Ryzhak, I. N. Kostyuchek, and Y. A. Tafeev, “Effect of tetrapeptide pancragene on functional morphology of the pancreas in rats with experimental diabetes mellitus,” Bull. Exp. Biol. Med., Vol. 143, nee. 3, pp. 368–371, maart 2007, doi: 10.1007/s10517-007-0114-y.
9. V. K. Khavinson et al., “[Tetrapeptide stimulates functional activity of the pancreatic cells in aging],” Adv. Gerontol. Uspekhi Gerontol., Vol. 25, nee. 4, pp. 680–684, 2012.
10. V. V. Ashapkin, N. S. Linkova, V. K. Khavinson, and B. F. Vanyushin, “Epigenetic mechanisms of peptidergic regulation of gene expression during aging of human cells,” Biochem. Biokhimiia, Vol. 80, nee. 3, pp. 310–322, maart 2015, doi: 10.1134/s0006297915030062.
11. V. K. Khavinson, N. A. Gavrisheva, V. V. Malinin, S. G. Chefu, and E. L. Trofimov, “Effect of pancragen on blood glucose level, capillary permeability and adhesion in rats with experimental diabetes mellitus,” Bull. Exp. Biol. Med., Vol. 144, nee. 4, pp. 559–562, oktober 2007, doi: 10.1007/s10517-007-0377-3.

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