Figure 2 Pathophysiology of hyperglycaemia in T2DM

Slides:

Advertisements

Similar presentations

What Causes Microvascular and Macrovascular Complications in Patients with Type 2 Diabetes? Charles A. Reasner, MD Professor of Medicine University of.

Advertisements

Stem Cells and Diabetes The Present. Background Diabetes affects more people and causes more deaths each year than breast cancer and AIDS combined. The.

Is it Diabetes Yet? If there is not enough insulin activity, or the body does not use the insulin effectively…. the body's blood glucose rises.

Insulin Pump Debrief. Now that you have worn a Pump… FAQ from people with diabetes Where do I wear this thing? What do I do with it when I play sports?

המנגנונים הקשורים בהתפתחות הסוכרת: ממחקר ליישום בבריאות האדם. אהוד זיו, היח' לסוכרת, הדסה עין כרם.

Insulin & Glucagon are synthesized in pancreatic islet cells Pancreas Small Intestine Pancreatic Duct Acini Cells Islet Cells Alpha Cells: secrete GLUCAGON.

The control of blood sugar 1. Blood sugar levels are higher than normal after a meal is digested. 2.

By Paige Pajarillo, Haley Duscha, and Emma Graley.

Insulin By: Zach Seabrook (Dedicated to Adam DeKoning)

Diabetes Mellitus Type 2

Diabetes. The Food You Eat is Broken Down Into Glucose to Supply Energy to Your Cells.

Diabetes. Warm Up Questions How many people do you know have diabetes? What is diabetes? Diabetes can be dangerous if it’s not treated. What happens if.

Fightdiabetes.com is a comprehensive website about diabetes. The mission of fightdiabetes.com is to inform, educate, discuss, guide you regarding diabetes.

Stages in the development of type 2 DM from a pre-diabetic, insulin-resistant state. As insulin sensitivity decreases, insulin-mediated glucose disposal.

Mean rates of insulin and glucagon delivery from an artificial pancreas at various blood glucose levels. The device was programmed to establish and maintain.

Type 1 Diabetes Mellitus

המשותף לכל סוגי הסוכרת היפרגליקמיה כרונית.

Ghrelin—a new player in glucose homeostasis?

with undiagnosed diabetes mellitus by three diagnostic criteria

Figure 4 Amino acid structure of short-acting and long-acting insulins

Nat. Rev. Endocrinol. doi: /nrendo

Figure 1 Mendelian randomization study

Nat. Rev. Endocrinol. doi: /nrendo

Figure 1 Candidate signalling pathways of irisin in adipocytes

Nat. Rev. Nephrol. doi: /nrneph

Figure 1 Monogenic forms of diabetes mellitus

Is Energy Deficiency Good in Moderation?

Nat. Rev. Cardiol. doi: /nrcardio

Figure 3 Putative actions of glucagon-like peptide 1 (GLP-1)

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Endocrinol. doi: /nrendo

Figure 3 Polysaccharides from plants and mushrooms

Figure 4 Effects of irisin on glucose homeostasis

Figure 2 Intracellular actions of metformin

Figure 1 Osteosarcoma epidemiology

Nat. Rev. Endocrinol. doi: /nrendo

Figure 2 Pharmacokinetic action profiles of rapid-acting insulins

Figure 2 Endocrine dysfunction in mitochondrial disease and their associated gene defects Figure 2 | Endocrine dysfunction in mitochondrial disease and.

Figure 3 Clinical algorithms in the management of NASH and diabetes mellitus Figure 3 | Clinical algorithms in the management of NASH and diabetes mellitus.

Figure 1 Simplified representation of the physiological

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Nephrol. doi: /nrneph

Figure 1 Regulation of hepatic glucose metabolism by the gut, brain and liver Figure 1 | Regulation of hepatic glucose metabolism by the gut, brain and.

Nat. Rev. Endocrinol. doi: /nrendo

IL-6 Muscles In on the Gut and Pancreas to Enhance Insulin Secretion

Figure 3 Pharmacodynamic action profiles of long-acting insulins

Dandan Wang et al. BTS 2018;3: Down-Regulation of miR-24 in Response to Insulin Infusion in Human Plasma Human plasma insulin (A), glucose (B),

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Endocrinol. doi: /nrendo

Figure 1 Sites of action of glucose-lowering agents

Figure 1 Physiological functions of leptin and ghrelin

Figure 2 Lipid metabolism and metabolism-disrupting chemicals.

Figure 4 Pathophysiological heterogeneity in patients with PCOS

Figure 2 Gut microbial gene content and development of T1DM

Figure 1 Timeline of pancreatic islet transplantation

Figure 1 Exercise enhances insulin sensitivity

Figure 5. Tissue uptake of circulating 125I-β2-m.

Figure 3 Global iodine status and mandatory salt iodization

The underlying physiological basis of the HOMA model.

ATL-801 treatment increases insulin sensitivity in KKAY mice.

Benjamin P. Garfinkel, Gökhan S. Hotamisligil Molecular Cell

Pathophysiology and drug targets.

Presentation transcript:

Figure 2 Pathophysiology of hyperglycaemia in T2DM Figure 2 | Pathophysiology of hyperglycaemia in T2DM. Insulin secretion from the β-cells in the pancreas normally reduces glucose output by the liver and increases glucose uptake by skeletal muscle and adipose tissue. Once β-cell dysfunction in the pancreas and/or insulin resistance in the liver, skeletal muscle or adipose tissue occur, hyperglycaemia develops, leading to an excessive amount of glucose circulating in the blood. The various factors listed at the top affect insulin secretion and insulin action. T2DM, type 2 diabetes mellitus. Zheng, Y. et al. (2017) Global aetiology and epidemiology of type 2 diabetes mellitus and its complications Nat. Rev. Endocrinol. doi:10.1038/nrendo.2017.151