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Incretin Based Therapies in Type 2 Diabetes Mellitus

Yıl 2017, Yıl: 2017 Sayı: 2, 174 - 180, 01.08.2017
https://doi.org/10.5505/kjms.2017.94830

Öz

For the treatment of T2DM; cure can not be achieved with conventional
methods. The degree of increase in the epidemic of diabetes;
together with the research of new treatments will provide a
better understanding of patophysiology necessitates the development.
Preferred drugs in cases that do not respond to metformin;
hypoglycemia, can cause weight gain and are undesirable cardiac
event. Today; incretin-based therapies have been developed that
provide effective glucose level and weight control. Incretins while
increasing glucose dependent insulin secretion in the pancreas,
suppress glucagon secretion.
Glucagon-like peptide-1 receptor agonists, and dipeptidyl peptidase-4
inhibitors, are incretin based treatment. Glucagon-like
peptide-1 receptor agonists is the most important treatment can
be used with monotherapy or combination therapy. Glucagon-like
peptide-1 agonists, besides providing good glycemic control, the
low rate of hypoglycemia and weight loss are causing significant
advantage. Dipeptidyl peptidase-4 inhibitors; leads to rapid inactivation
of incretin hormones such as glucagon-like peptide-1
agonists and glucose dependent insulinotropic polypeptide.
Dipeptidyl peptidase-4 inhibitors; they extend the duration of action
of glucagon-like peptide-1 by inhibiting the degradation of incretin
hormones in circulation

Kaynakça

  • 1. Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care 2004;27:1047–53.
  • 2. Stonehouse AH, Darsow T, Maggs DG. Incretin-based therapies. J Diabetes 2012;4:55–67.
  • 3. McIntosh CH, Demuth HU, Pospisilik JA, Pederson R. Dipeptidyl peptidase IV inhibitors: how do they work as new antidiabetic agents? Regul Pept 2005;128:159–65.
  • 4. Creutzfeldt W. The incretin concept today. Diabetol 1979;16:75–85.
  • 5. Nauck MA, Homberger E, Siegel EG, Allen RC, Eaton RP, Ebert R et al. Incretin effects of increasing glucose loads in man calculated from venous insulin and C-peptide responses. J Clin Endocrinol Metab 1986;63:492–8.
  • 6. Holst JJ. Glucagon-like peptide-1: from extract to agent. The Claude Bernard Lecture. Diabetol 2006;49:253–60.
  • 7. Eissele R, Göke R, Willemer S, Harthus HP, Vermeer H, Arnold R, et al. Glucagon-like peptide-1 cells in the gastrointestinal tract and pancreas of rat, pig and man. Eur J Clin Invest 1992;22:283–91.
  • 8. Deacon CF, Pridal L, Klarskov L, Olesen M, Holst JJ. Glucagonlike peptide 1 undergoes differential tissue-specific metabolism in the anesthetized pig. Am J Physiol 1996;271:458–64.
  • 9. Vilsboll T, Agersø H, Krarup T, Holst JJ. Similar elimination rates of glucagon-like peptide-1 in obese type 2 diabetic patients and healthy subjects. J Clin Endocrinol Metab 2003;88:220–4.
  • 10. Deacon CF, Nauck MA, Meier J, Hücking K, Holst JJ. Degradation of endogenous and exogenous gastric inhibitory polypeptide in healthy and in type 2 diabetic subjects as revealed using a new assay for the intact peptide. J Clin Endocrinol Metab 2000;85:3575–81.
  • 11. Vilsboll T, Agersø H, Lauritsen T, Deacon CF, Aaboe K, Madsbad S, et al. The elimination rates of intact GIP as well as its primary metabolite, GIP 3–42, are similar in type 2 diabetic patients and healthy subjects. Regul Pept 2006;137:168–72.
  • 12. Deacon CF, Johnsen AH, Holst JJ. Degradation of glucagonlike peptide-1 by human plasma in vitro yields an Nterminally truncated peptide that is a major endogenous metabolite in vivo. J Clin Endocrinol Metab 1995;80:952–7.
  • 13. Deacon CF, Nauck MA, Toft-Nielsen M, Pridal L, Willms B, Holst JJ. Both subcutaneously and intravenously administered glucagon-like peptide I are rapidly degraded from the NH2- terminus in type II diabetic patients and in healthy subjects. Diabetes 1995;44:1126–31.
  • 14. Holst JJ, Deacon CF. Inhibition of the activity of dipeptidylpeptidase IV as a treatment for type 2 diabetes. Diabetes 1998;47:1663–70.
  • 15. Elliott RM, Morgan LM, Tredger JA, Deacon S, Wright J, Marks V. Glucagon-like peptide-1(7–36)amide and glucosedependent insulinotropic polypeptide secretion in response to nutrient ingestion in man: acute post-prandial and 24-h secretion patterns. J Endocrinol 1993;138:159–66.
  • 16. Orskov C, Wettergren A, Holst JJ. Secretion of the incretin hormones glucagon-like peptide-1 and gastric inhibitory polypeptide correlates with insulin secretion in normal man throughout the day. Scand J Gastroenterol 1996;31:665–70.
  • 17. Ahren B, Carr RD, Deacon CF. Incretin hormone secretion over the day. Vitam Horm 2010;84:203–20.
  • 18. Deacon CF. What do we know about the secretion and degradation of incretin hormones? Regul Pept 2005;128:117–24.
  • 19. Lindgren O, Mari A, Deacon CF, Carr RD, Winzell MS, Vikman J, et al. Differential islet and incretin hormone responses in morning versus afternoon after standardized meal in healthy men. J Clin Endocrinol Metab 2009;94:2887–92.
  • 20. Baggio LL, Drucker DJ. Biology of incretins: GLP-1 and GIP. Gastroenterol 2007;132:2131–57.
  • 21. Schirra J, Nicolaus M, Roggel R, Katschinski M, Storr M, Woerle HJ, et al. Endogenous glucagon-like peptide 1 controls endocrine pancreatic secretion and antropyloro-duodenal motility in humans. Gut 2006;55:243–51
  • 22. Nauck MA, Niedereichholz U, Ettler R, Holst JJ, Orskov C, Ritzel R, et al. Glucagon-like peptide 1 inhibition of gastric emptying outweighs its insulinotropic effects in healthy humans. Am J Physiol 1997;273:981–8.
  • 23. Verdich C, Flint A, Gutzwiller JP, Näslund E, Beglinger C, Hellström PM, et al. A meta-analysis of the effect of glucagonlike peptide-1(7–36)amide on ad libitum energy intake in humans. J Clin Endocrinol Metab 2001;86:4382–9.
  • 24. Madsbad S, Krarup T, Deacon CF, Holst JJ. Glucagon- like peptide receptor agonists and dipeptidyl peptidase-4 inhibitors in the treatment of diabetes: a review of clinical trials. Curr Opin Clin Nutr Metab Care 2008;11:491–9.
  • 25. Muscelli E, Mari A, Casolaro A, Camastra S, Seghieri G, Gastaldelli A, et al. Separate impact of obesity and glucose tolerance on the incretin effect in normal subjects and type 2 diabetic patients. Diabetes 2008;57:1340–8.
  • 26. Knop FK, Aaboe K, Vilsboll T, Volund A, Madsbad S, Holst JJ, et al. Reduced incretin effect in obese subjects with normal glucose tolerance as compared to lean control subjects. Diabetes 2008;57:410.
  • 27. Carr RD, Larsen MO, Jelic K, Lindgren O, Vikman J, Holst JJ, et al. Secretion and dipeptidyl peptidase-4-mediated metabolism of incretin hormones after a mixed meal or glucose ingestion in obese compared to lean, nondiabetic men. J Clin Endocrinol Metab 2010;95:872–8.
  • 28. Toft-Nielsen MB, Damholt MB, Madsbad S, Hilsted LM, Hughes TE, Michelsen BK, et al. Determinants of the impaired secretion of glucagon-like peptide-1 in type 2 diabetic patients. J Clin Endocrinol Metab 2001;86:3717–23.
  • 29. Vollmer K, Holst JJ, Baller B, Ellrichmann M, Nauck MA, Schmidt WE, et al. Predictors of incretin concentrations in subjects with normal, impaired, and diabetic glucose tolerance. Diabetes 2008;57:678–87.
  • 30. Nauck M, Stockmann F, Ebert R, Creutzfeldt W. Reduced incretin effect in type 2(non-insulin-dependent) diabetes. Diabetol 1986;29:46–52.
  • 31. Bagger JI, Knop FK, Lund A, Vestergaard H, Holst JJ, Vilsbøll T. Impaired regulation of the incretin effect in patients with type 2 diabetes. J Clin Endocrinol Metab 2011;96:737–45.
  • 32. Chiniwala N, Jabbour S. Management of diabetes mellitus in the elderly. Curr Opin Endocrinol Diabetes Obes 2011:18:148–52. 33. Rodbard HW, Jellinger PS, Davidson JA, Einhorn D, Garber AJ, Grunberger G, et al. Statement by an American Association of Clinical Endocrinologists/American College of Endocrinology consensus panel on type 2 diabetes mellitus: an algorithm for glycemic control. Endocr Pract 2009;15:540–59.
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Diabetes Mellitus Tip 2’de İnkretin Temelli Tedaviler

Yıl 2017, Yıl: 2017 Sayı: 2, 174 - 180, 01.08.2017
https://doi.org/10.5505/kjms.2017.94830

Öz

Diyabet tedavisinde, geleneksel yöntemlerle kür sağlanamamaktadır.
Diyabetin salgın derecesinde artışı patofizyolojsinin daha iyi
anlaşılmasını sağlayacak araştırmalarla birlikte yeni tedavilerin geliştirilmesini
zorunlu kılmaktadır. Metformin tedavisine cevap vermeyen
durumlarda tercih edilen ilaçlar; hipoglisemi, kilo alımı ve
istenmeyen kardiak olaylara neden olabilmektedirler. Günümüzde
etkin glukoz ve kilo kontrolü sağlayan inkretin bazlı tedaviler geliştirilmiştir.
İnkretinler pankreasta glukoza bağımlı insülin sekresyonunu
artırırken, glukagon sekresyonunu baskılar.Glukagon benzeri peptid-1 reseptör agonistleri ve dipeptidil peptidaz-4
inhibitörleri inkretin bazlı tedavilerdir. Glukagon benzeri
peptid-1 reseptör agonistleri önemli tedavilerden olup, monoterapi
veya kombine tedavilerle birlikte kullanılabilmektedir. İyi glisemik
kontrol sağlamalarının yanında hipoglisemi oranların düşük olması
ve kilo kaybına neden olmaları önemli avantajlarıdır. Dipeptidil
peptidaz-4 inhibitörleri; glukagon benzeri peptid-1 ve glukoz ba-
ğımlı insülinotropik polipeptid gibi inkretin hormonların hızlıca inaktivasyonuna
neden olur. DPP-4 inhibitörleri; dolaşımdaki inkretin
hormonların yıkım

Kaynakça

  • 1. Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care 2004;27:1047–53.
  • 2. Stonehouse AH, Darsow T, Maggs DG. Incretin-based therapies. J Diabetes 2012;4:55–67.
  • 3. McIntosh CH, Demuth HU, Pospisilik JA, Pederson R. Dipeptidyl peptidase IV inhibitors: how do they work as new antidiabetic agents? Regul Pept 2005;128:159–65.
  • 4. Creutzfeldt W. The incretin concept today. Diabetol 1979;16:75–85.
  • 5. Nauck MA, Homberger E, Siegel EG, Allen RC, Eaton RP, Ebert R et al. Incretin effects of increasing glucose loads in man calculated from venous insulin and C-peptide responses. J Clin Endocrinol Metab 1986;63:492–8.
  • 6. Holst JJ. Glucagon-like peptide-1: from extract to agent. The Claude Bernard Lecture. Diabetol 2006;49:253–60.
  • 7. Eissele R, Göke R, Willemer S, Harthus HP, Vermeer H, Arnold R, et al. Glucagon-like peptide-1 cells in the gastrointestinal tract and pancreas of rat, pig and man. Eur J Clin Invest 1992;22:283–91.
  • 8. Deacon CF, Pridal L, Klarskov L, Olesen M, Holst JJ. Glucagonlike peptide 1 undergoes differential tissue-specific metabolism in the anesthetized pig. Am J Physiol 1996;271:458–64.
  • 9. Vilsboll T, Agersø H, Krarup T, Holst JJ. Similar elimination rates of glucagon-like peptide-1 in obese type 2 diabetic patients and healthy subjects. J Clin Endocrinol Metab 2003;88:220–4.
  • 10. Deacon CF, Nauck MA, Meier J, Hücking K, Holst JJ. Degradation of endogenous and exogenous gastric inhibitory polypeptide in healthy and in type 2 diabetic subjects as revealed using a new assay for the intact peptide. J Clin Endocrinol Metab 2000;85:3575–81.
  • 11. Vilsboll T, Agersø H, Lauritsen T, Deacon CF, Aaboe K, Madsbad S, et al. The elimination rates of intact GIP as well as its primary metabolite, GIP 3–42, are similar in type 2 diabetic patients and healthy subjects. Regul Pept 2006;137:168–72.
  • 12. Deacon CF, Johnsen AH, Holst JJ. Degradation of glucagonlike peptide-1 by human plasma in vitro yields an Nterminally truncated peptide that is a major endogenous metabolite in vivo. J Clin Endocrinol Metab 1995;80:952–7.
  • 13. Deacon CF, Nauck MA, Toft-Nielsen M, Pridal L, Willms B, Holst JJ. Both subcutaneously and intravenously administered glucagon-like peptide I are rapidly degraded from the NH2- terminus in type II diabetic patients and in healthy subjects. Diabetes 1995;44:1126–31.
  • 14. Holst JJ, Deacon CF. Inhibition of the activity of dipeptidylpeptidase IV as a treatment for type 2 diabetes. Diabetes 1998;47:1663–70.
  • 15. Elliott RM, Morgan LM, Tredger JA, Deacon S, Wright J, Marks V. Glucagon-like peptide-1(7–36)amide and glucosedependent insulinotropic polypeptide secretion in response to nutrient ingestion in man: acute post-prandial and 24-h secretion patterns. J Endocrinol 1993;138:159–66.
  • 16. Orskov C, Wettergren A, Holst JJ. Secretion of the incretin hormones glucagon-like peptide-1 and gastric inhibitory polypeptide correlates with insulin secretion in normal man throughout the day. Scand J Gastroenterol 1996;31:665–70.
  • 17. Ahren B, Carr RD, Deacon CF. Incretin hormone secretion over the day. Vitam Horm 2010;84:203–20.
  • 18. Deacon CF. What do we know about the secretion and degradation of incretin hormones? Regul Pept 2005;128:117–24.
  • 19. Lindgren O, Mari A, Deacon CF, Carr RD, Winzell MS, Vikman J, et al. Differential islet and incretin hormone responses in morning versus afternoon after standardized meal in healthy men. J Clin Endocrinol Metab 2009;94:2887–92.
  • 20. Baggio LL, Drucker DJ. Biology of incretins: GLP-1 and GIP. Gastroenterol 2007;132:2131–57.
  • 21. Schirra J, Nicolaus M, Roggel R, Katschinski M, Storr M, Woerle HJ, et al. Endogenous glucagon-like peptide 1 controls endocrine pancreatic secretion and antropyloro-duodenal motility in humans. Gut 2006;55:243–51
  • 22. Nauck MA, Niedereichholz U, Ettler R, Holst JJ, Orskov C, Ritzel R, et al. Glucagon-like peptide 1 inhibition of gastric emptying outweighs its insulinotropic effects in healthy humans. Am J Physiol 1997;273:981–8.
  • 23. Verdich C, Flint A, Gutzwiller JP, Näslund E, Beglinger C, Hellström PM, et al. A meta-analysis of the effect of glucagonlike peptide-1(7–36)amide on ad libitum energy intake in humans. J Clin Endocrinol Metab 2001;86:4382–9.
  • 24. Madsbad S, Krarup T, Deacon CF, Holst JJ. Glucagon- like peptide receptor agonists and dipeptidyl peptidase-4 inhibitors in the treatment of diabetes: a review of clinical trials. Curr Opin Clin Nutr Metab Care 2008;11:491–9.
  • 25. Muscelli E, Mari A, Casolaro A, Camastra S, Seghieri G, Gastaldelli A, et al. Separate impact of obesity and glucose tolerance on the incretin effect in normal subjects and type 2 diabetic patients. Diabetes 2008;57:1340–8.
  • 26. Knop FK, Aaboe K, Vilsboll T, Volund A, Madsbad S, Holst JJ, et al. Reduced incretin effect in obese subjects with normal glucose tolerance as compared to lean control subjects. Diabetes 2008;57:410.
  • 27. Carr RD, Larsen MO, Jelic K, Lindgren O, Vikman J, Holst JJ, et al. Secretion and dipeptidyl peptidase-4-mediated metabolism of incretin hormones after a mixed meal or glucose ingestion in obese compared to lean, nondiabetic men. J Clin Endocrinol Metab 2010;95:872–8.
  • 28. Toft-Nielsen MB, Damholt MB, Madsbad S, Hilsted LM, Hughes TE, Michelsen BK, et al. Determinants of the impaired secretion of glucagon-like peptide-1 in type 2 diabetic patients. J Clin Endocrinol Metab 2001;86:3717–23.
  • 29. Vollmer K, Holst JJ, Baller B, Ellrichmann M, Nauck MA, Schmidt WE, et al. Predictors of incretin concentrations in subjects with normal, impaired, and diabetic glucose tolerance. Diabetes 2008;57:678–87.
  • 30. Nauck M, Stockmann F, Ebert R, Creutzfeldt W. Reduced incretin effect in type 2(non-insulin-dependent) diabetes. Diabetol 1986;29:46–52.
  • 31. Bagger JI, Knop FK, Lund A, Vestergaard H, Holst JJ, Vilsbøll T. Impaired regulation of the incretin effect in patients with type 2 diabetes. J Clin Endocrinol Metab 2011;96:737–45.
  • 32. Chiniwala N, Jabbour S. Management of diabetes mellitus in the elderly. Curr Opin Endocrinol Diabetes Obes 2011:18:148–52. 33. Rodbard HW, Jellinger PS, Davidson JA, Einhorn D, Garber AJ, Grunberger G, et al. Statement by an American Association of Clinical Endocrinologists/American College of Endocrinology consensus panel on type 2 diabetes mellitus: an algorithm for glycemic control. Endocr Pract 2009;15:540–59.
  • 34. Ghatak SB, Patel DS, Shanker N, Srivstava A, Deshpande SS, Panchal SJ. Alogliptin: a novel molecule for improving glycemic control in type II diabetes mellitus. Curr Diabetes Rev 2010;6:410–21.
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  • 46. Buse J, Rosenstock J, Sesti G, Schmidt WE, Montanya E, Brett JH, et al. Liraglutide once a day versus exenatide twice a day for type 2 diabetes: a 26-week randomised, parallelgroup, multinational, open-label trial (LEAD-6). Lancet 2009;374:39–47.
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Toplam 78 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Konular Klinik Tıp Bilimleri
Bölüm Derleme
Yazarlar

Uğur Alp Göksu

Aysun Ünal Bu kişi benim

Yayımlanma Tarihi 1 Ağustos 2017
Yayımlandığı Sayı Yıl 2017 Yıl: 2017 Sayı: 2

Kaynak Göster

APA Göksu, U. A., & Ünal, A. (2017). Diabetes Mellitus Tip 2’de İnkretin Temelli Tedaviler. Kafkas Journal of Medical Sciences, 7(2), 174-180. https://doi.org/10.5505/kjms.2017.94830
AMA Göksu UA, Ünal A. Diabetes Mellitus Tip 2’de İnkretin Temelli Tedaviler. KAFKAS TIP BİL DERG. Ağustos 2017;7(2):174-180. doi:10.5505/kjms.2017.94830
Chicago Göksu, Uğur Alp, ve Aysun Ünal. “Diabetes Mellitus Tip 2’de İnkretin Temelli Tedaviler”. Kafkas Journal of Medical Sciences 7, sy. 2 (Ağustos 2017): 174-80. https://doi.org/10.5505/kjms.2017.94830.
EndNote Göksu UA, Ünal A (01 Ağustos 2017) Diabetes Mellitus Tip 2’de İnkretin Temelli Tedaviler. Kafkas Journal of Medical Sciences 7 2 174–180.
IEEE U. A. Göksu ve A. Ünal, “Diabetes Mellitus Tip 2’de İnkretin Temelli Tedaviler”, KAFKAS TIP BİL DERG, c. 7, sy. 2, ss. 174–180, 2017, doi: 10.5505/kjms.2017.94830.
ISNAD Göksu, Uğur Alp - Ünal, Aysun. “Diabetes Mellitus Tip 2’de İnkretin Temelli Tedaviler”. Kafkas Journal of Medical Sciences 7/2 (Ağustos 2017), 174-180. https://doi.org/10.5505/kjms.2017.94830.
JAMA Göksu UA, Ünal A. Diabetes Mellitus Tip 2’de İnkretin Temelli Tedaviler. KAFKAS TIP BİL DERG. 2017;7:174–180.
MLA Göksu, Uğur Alp ve Aysun Ünal. “Diabetes Mellitus Tip 2’de İnkretin Temelli Tedaviler”. Kafkas Journal of Medical Sciences, c. 7, sy. 2, 2017, ss. 174-80, doi:10.5505/kjms.2017.94830.
Vancouver Göksu UA, Ünal A. Diabetes Mellitus Tip 2’de İnkretin Temelli Tedaviler. KAFKAS TIP BİL DERG. 2017;7(2):174-80.