Im Bereich der oralen Diabetestherapie, der Insulinpräparate und –applikationen sowie
der Blutzuckerselbstkontrolle gab es in den vergangenen Jahren wesentliche Weiterentwicklungen.
Trotz dieser Fortschritte ist bei einem großen Teil der Typ–2–Diabetiker der Blutzucker
nur unzureichend eingestellt. Außerdem können die bisher verfügbaren oralen Antidiabetika
den Diabetes weder heilen noch die Betazellfunktion oder den Stoffwechsel komplett
wiederherstellen bzw. das kardiovaskuläre Risiko auf ein normales Maß reduzieren.
Diese Defizite rechtfertigen die weitere Entwicklung innovativer Therapieoptionen.
Zu den in den vergangenen Jahren neu entwickelten Strategien zählen vor allem die
Nutzung des Inkretineffekts als Basis für neue Antidiabetika wie Inkretinmimetika,
GLP–1–Analoga und DPP–4–Hemmer und die selektive Blockade von Rezeptoren des Endocannabinoidsystems.
Recent years have seen further major advances in the oral treatment of diabetes, insulins
and their application, and in self–measurement of blood glucose levels. Nevertheless,
glucose levels in a large number of type 2 diabetics are inadequately adjusted. Furthermore,
the currently available oral antidiabetic agents are unable to effect a cure, completely
restore beta cell function or metabolism, or even reduce the cardiovascular risk to
normal levels. In view of these deficiencies, the further development of innovative
therapeutic options is justified. Among the newly developed strategies of recent years,
the utilisation of the incretin effect as a basis for new antidiabetics such as incretin
mimetics, GLP–1 analogues and DPP–4 inhibitors, and the selective endocannabinoid
receptor blockers deserves particular mention.
Key words
type 2 diabetes - beta cell function - cardiovascular risk - incretin effect - incretin
mimetics - GLP–1 analogues - DPP–4 inhibitors - endogenous cannabinoid system
Literatur
- 1
Zimmet P. et al. .
Global and societal implications of the diabetes epidemic.
Nature.
2001;
414
782-787
- 2
McCarthy MI..
Growing evidence for diabetes susceptibility genes from genome scan data.
Curr Diab Rep.
2003;
3
159-167
- 3
Rathmann W. et al. .
High prevalence of undiagnosed diabetes mellitus in Southern Germany: target populations
for efficient screening. The KORA survey 2000.
Diabetologia.
2003;
46
182-189
- 4
Icks A. et al. .
Versorgungsqualität und Ausmaß von Komplikationen an einer bevölkerungsbezogenen Stichprobe
von Typ–2–Diabetespatienten.
Dtsch Med Wochenschr.
2006;
131
73-78
- 5
Meier JJ. et al. .
Neue Konzepte in der Behandlung des Typ–2–Diabetes.
Internist (Berl) 2007.
2007;
698
700-707
- 6
Blüher M. et al. .
Adipositas und Metabolisches Syndrom.
Diabetologie.
2008;
3
- 7
Effect of intensive blood–glucose control with metformin on complications in overweight
patients with type 2 diabetes (UKPDS 34). UK Prospective Diabetes Study (UKPDS) Group.
Lancet.
1998;
352
854-865
- 8
Dormandy JA. et al. .
Secondary prevention of macrovascular events in patients with type 2 diabetes in the
PROactive Study (PROspective pioglitAzone Clinical Trial In macroVascular Events):
a randomised controlled trial.
Lancet.
2005;
366
1279-1289
- 9
Nauck MA. et al. .
Gastric inhibitory polypeptide and glucagon–like peptide–1 in the pathogenesis of
type 2 diabetes.
Diabetes.
2004;
53
- 10
Drucker DJ. et al. .
The incretin system: glucagon–like peptide–1 receptor agonists and dipeptidyl peptidase–4
inhibitors in type 2 diabetes.
Lancet.
2006;
368
1696-1705
- 11
Pi–Sunyer FX. et al. .
Efficacy and tolerability of vildagliptin monotherapy in drug–naive patients with
type 2 diabetes.
Diabetes Res Clin Pract.
2007;
76
132-138
- 12
Bosi E. et al. .
Effects of vildagliptin on glucose control over 24 weeks in patients with type 2 diabetes
inadequately controlled with metformin.
Diabetes Care.
2007;
30
890-895
- 13
Abel EL..
Cannabis: effects on hunger and thirst.
Behav Biol.
1975;
15
255-281
- 14
Pagotto U. et al. .
The emerging role of the endocannabinoid system in endocrine regulation and energy
balance.
Endocr Rev.
2006;
27
73-100
- 15
Munro S. et al. .
Molecular characterization of a peripheral receptor for cannabinoids.
Nature.
1993;
365
61-65
- 16
Wierzbicki AS..
Rimonabant: endocannabinoid inhibition for the metabolic syndrome.
Int J Clin Pract.
2006;
60
1697-1706
- 17
Pi–Sunyer FX. et al. .
Effect of rimonabant, a cannabinoid–1 receptor blocker, on weight and cardiometabolic
risk factors in overweight or obese patients: RIO–North America: a randomized controlled
trial.
JAMA.
2006;
295
761-775
- 18
Van Gaal LF. et al. .
Effects of the cannabinoid–1 receptor blocker rimonabant on weight reduction and cardiovascular
risk factors in overweight patients: 1–year experience from the RIO–Europe study.
Lancet.
2005;
365
1389-1397
- 19
Després JP. et al. .
Effects of rimonabant on metabolic risk factors in overweight patients with dyslipidemia.
N Engl J Med.
2005;
353
2121-2134
- 20
Scheen AJ. et al. .
Efficacy and tolerability of rimonabant in overweight or obese patients with type
2 diabetes: a randomised controlled study.
Lancet.
2006;
368
1660-1672
- 21
Nissen SE. et al. .
Effect of rimonabant on progression of atherosclerosis in patients with abdominal
obesity and coronary artery disease: the STRADIVARIUS randomized controlled trial.
JAMA.
2008;
299
1547-1560
- 22 EMEA. .Questions and answers on the recommendation to suspend the marketing authorisation
of Accomplia® (rimonabant), 23. Oktober 2008.
www.emea.europa.eu/humandocs/PDFs/EPAR/acomplia/53715308en.pdf
1 KOoperative gesundheitsforschung in der Region Augsburg
2 United Kingdom Prospective Diabetes Study
3 STudies with Rimonabant And Tobacco Use
4 Rimonabant In Overweight/Obesity
Korrespondenz
Prof. Dr. Matthias Blüher
Medizinische Klinik und Poliklinik III Universität Leipzig
Philipp–Rosenthal–Straße 27
04103 Leipzig
eMail: bluma@medizin.uni-leipzig.de
