Pathophysiology of insulin resistance in type 2 diabetes genetic,jan 1 1970 how to fix,january git lyrics - Test Out

OAD Producten die de gevoeligheid voor insuline verhogen + daling glycogenolyse thv lever Biguaniden (vb. SGLT2 Inhibition: A Novel Approach to Reduce Hyperglycaemia SGLT2 inhibition decreases plasma glucose by increasing urinary glucose excretion Canagliflozin is a potent inhibitor of SGLT2 Rothenberg PL et al.
Take home messages ? Medicatie aanpassen aan de nierfunctie ? Geen combinatie SU met gliniden ? Geen insulinesecretie :overschakelen naar insuline ? Medicatie aanpassen aan ptn: risico op hypoglycemies en gewichtstoename !
Pancreas Actief GLP-1 (7-36) Inactief GLP-1 (9-36) amide 2 aminozuren afgesplitst van het amino-uiteinde Vermindert de afgifte van glucose door de lever, waardoor de glucosecontrole verbetert Verhoogt het glucosegebruik door de spieren en het vetweefsel Glucoseafhankelijke onderdrukking van glucagon ?-cellen Glucoseafhankelijke insulinesecretie ?-cellen Voedselinname DarmenDPP-4 Werkingsmechanisme DPP-4 inhibitie Aangepast naar Drucker DJ. Take home message Vroegtijdige metabole controle is belangrijk Tijdig insuline opstarten zonodig OPTITREREN tot streefwaarde (zoek naar patronen) mag al na 3 dagen!!
Richtlijnen voor diabeten Gezonde, evenwichtige voeding Speciale aandacht voor koolhydraten, vetten en energiebehoefte.
Najaarsvorming dietisten Een organisatie van de Vlaamse Diabetesvereniging vzw & Vlaamse Vereniging van Voedingskundigen en Dietisten in samenwerking met.
Link between type 2 diabetes, insulin resistance and increased breast cancer risk of development: pathophysiology. Tufts OCW material is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported License.
Insulin resistance is a condition that develops when we eat too much sugar or refined carbohydrates, don’t exercise, are under high amounts of stress on a regular basis and gain excess weight, especially abdominal fat. Our current approach to prevention and treatment is obviously not working because millions more are affected every year.  Not too long ago, this health condition was extremely rare.  How does diabetes impact our health?
According to a recent study, people in their 50’s with diabetes may age before their time compared with their diabetes-free counterparts! Although insulin resistance is most closely associated with the development of type 2 diabetes and its associated age-related health problems as described above, unfortunately, it doesn’t stop there.  Insulin resistance also increases your risk of developing all of the following health conditions as well. There is increasing evidence in the literature regarding the role excess insulin plays in carcinogenesis (initiation of cancer) for various types of cancer.[77] [78] The studies are becoming more conclusive on insulin’s role in promoting inflammatory responses and its numerous adverse impacts on human metabolism.
Type 2 diabetes • Characterized by chronic hyperglycemia • Associated with microvascular and macrovascular complications • General y arises from a combination of insulin resistance and ?-cel dysfunction Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications. Insulin resistance and ?-cel dysfunction are core defects of type 2 diabetes Genetic susceptibility, obesity, Western lifestyle Insulin resistance IR ?-cell ? dysfunction Type 2 diabetes Rhodes CJ & White MF. Overal , 75% of patients with type 2 diabetes die from cardiovascular disease Gray RP & Yudkin JS. Insulin resistance is closely linked to cardiovascular disease Present in > 80% of people with type 2 diabetes1 Approximately doubles Insulin IR the risk of a cardiac event2 resistance Implicated in almost half of CHD events in individuals with type 2 diabetes2 1Haffner SM, et al. Insulin resistance is linked to a range of cardiovascular risk factors Hyperglycemia Dyslipidemia Hypertension Insulin IR resistance Damage to blood vessels Clotting abnormalities Atherosclerosis Inflammation Zimmet P. Glycemic control declines over time Diet Sulfonylurea or insulin 9 )(% 1c 8 Ab H ian ed 7 M 6.2% upper limit of normal range 60 0 3 6 9 12 15 Years from randomization UK Prospective Diabetes Study (UKPDS) Group. Loss of ?-cell function occurs before diagnosis 100 Up to ) 80 Diagnosis 50% (%n loss 60 ctio n 40 ?-cell fu 20 0 -10 -9 -8 -7 -6 -5 -4 -3 -2 -1 1 2 3 4 5 6 Time from diagnosis (years) Holman RR. The dual action of thiazolidinediones reduces HbA1c Insulin ?-cell resistance IR + ? function HbA1c Lebovitz HE, et al. Insulin sensitizers reduce cardiovascular events in type 2 diabetes ) 60 50 t rate (% 40 even edin 30 bm co 20 thno 10 12-m 0 Non-sensitizers Sensitizers Kao JA, et al.


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Metformine®, Glucophage®) Metformax®) ? weinig risico op hypo ? innametijdstip : tijdens of net na de maaltijd Glitazones (vb. Invokana®) ? risico op genitale infecties ? innametijdstip : voor de maaltijd ? Minder kans op hypoglycemies ? Gewichtsafname ! Incretine effect Bij voedsel innamen : Insuline Glucagon Glucagon GLP-1 (= hormoon uit darm) GLP-1 (= hormoon uit.
Effect of alterations of the specific activity of the intracellular acetyl CoA pool apparent rates of hepatic cholesterogenesis. The cardiovascular risk factor plasminogen activator inhibitor type I is related to insulin resistance.
Fibrinolytic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. Women with polycystic ovary syndrome have intrinsic insulin resistance on euglycaemic-hyperinsulaemic clamp.  Hum Reprod. Women with polycystic ovary syndrome wedge resected in 1956 to 1965: a long term follow-up focusing on natural history and circulating hormones. Metabolic lessons from the study of young adolescents with polycystic ovary syndrome, is insulin indeed the culprit. Glucocorticoids as counterregulatory hormones of leptin: toward an understanding of leptin resistance.
Glutathione (GSH) and the GSH synthesis gene Gclm modulate vascular reactivity in mice.  Free Radic Biol Med. Novel link between inflammation, endothelial dysfunction, and muscle insulin resistance.   Diabetes. If you interesting in "Targeting the Underlying Pathophysiology of Type 2 Diabetes" powerpoint themes, you can download to use this powerpoint template for your own presentation template. Department of Noncommunicable Disease Surveillance, World Health Organization, Geneva 1999.
Normal IGT* Type 2 diabetes Insulin Increased insulin resistance resistance Insulin Hyperinsulinemia, secretion then ?-cell failure Post- Abnormal prandial glucose tolerance glucose Fasting glucose Hyperglycemia *IGT = impaired glucose tolerance Adapted from Type 2 Diabetes BASICS. Oversecretion of insulin to compensate for insulin resistance1,2 Glucotoxicity2 Lipotoxicity3 Chronic Pancreas High circulating hyperglycemia free fatty acids ?-cell dysfunction 1Boden G & Shulman GI. The Global Partnership recommends: Address the underlying pathophysiology, including treatment of insulin resistance Del Prato S, et al. We examined the restoration of first-phase and total insulin response as well as hepatic and peripheral insulin sensitivity. For adults aged 51-60 with diabetes, the odds of developing new geriatric conditions were nearly double those who didn’t have diabetes! Alzheimer Research Forum live discussion: Insulin resistance: a common axis linking Alzheimer’s, depression and metabolism? For viewing only, you can play with our flash based presentation viewer instead of downloading the ppt file.
Additionally, to examine the mechanistic basis of observed outcomes, we quantified the change in fat content of the pancreas and liver The data are consistent with the hypothesis that the abnormalities of insulin secretion and insulin resistance that underlie type 2 diabetes have a single, common aetiology, i.e.


This provides a unified hypothesis to explain a common disease that previously appeared to require separate disease processes affecting the pancreas and insulin-sensitive tissues. Prior to the onset of spontaneous diabetes in rodents, both total pancreatic fat and islet triacylglycerol content increase sharply. In vitro, chronic saturated fatty acid exposure of beta cells inhibits the acute insulin response to glucose, and removal of fatty acids allows recovery of this response. The present data provide clear evidence that decreasing total pancreatic fat is associated with a return of beta cell function. However, it is probable that the negative effect on beta cell function is exerted by toxic intermediaries such as diacylglycerol and ceramides, which change rapidly in response to acute metabolic changes, rather than by stored triacylglycerol per se, which acts as an index of fatty acid intermediary concentration. Endless access to abundant calories from carbohydrate may be an evolutionarily novel, and thus pathology-inducing, situation.
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Normal weight and occasionally fasting people probably won't increase their longevity further by severe caloric restriction.
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Comments to Pathophysiology of insulin resistance in type 2 diabetes genetic

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