T2D

fatimaelfitouri
Mind Map by fatimaelfitouri, updated more than 1 year ago
fatimaelfitouri
Created by fatimaelfitouri almost 6 years ago
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Diabetes Mind Map on T2D, created by fatimaelfitouri on 04/06/2014.
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Resource summary

T2D
1 insulin
1.1 how does insulin affect metabolic pathways and how it influences energy balance
1.2 glucagon as anatagonist effects to insulin
1.3 Physiologically, pancreatic b-cells constantly synthesize insulin, regardless of blood glucose levels. Insulin is stored within vacuoles and released once triggered by an elevation of the blood glucose
1.4 Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells, including skeletal muscle cells and adipocytes.
1.5 Insulin is also the major signal for conversion of glucose to glycogen for internal storage in liver and skeletal muscle cells
1.6 Insulin has autacoid (stimulatory) and chalone (inhibitory) actions
1.7 Insulin promotes glucose uptake by stimulating the translocation of GLUT4 from intracellular sites
1.8 increases the activity of several enzymes in the glycolytic pathway including glucokinase
1.9 Insulin does not stimulate glucose uptake in the liver, it inhibits glycogenolysis and gluconeogenesis
1.10 Insulin up regulates transcription of PFK, PK and PDH
1.11 Differentiation of adipocytes is insulin dependent
1.12 Insulin inhibits HSL (hormone sensitive lipase). HSL breaks down TG to FA
2 common features
2.1 impaired glucose handing caused by dyslipidemia
2.1.1 Dyslipidemia
2.1.1.1 characteristic features of this phenotype are a high plasma triglyceride concentration, low HDL cholesterol concentration and increased concentration of small dense LDL–cholesterol particles.
2.1.1.1.1 the prevalence of high plasma triglyceride and low HDLs levels in individuals with diabetes mellitus is significantly higher than in those without diabetes mellitus
2.1.1.2 insulin resistance has a central role in the development of diabetic dyslipidemia The main cause of the three cardinal features (high TAGs, low HDL and high LDL) of diabetic dyslipidemia is the increased free fatty-acid release from insulin-resistant fat cells
2.1.1.2.1 The increased flux of free fatty acids into the liver in the presence of adequate glycogen stores promotes triglyceride production, which in turn stimulates the secretion of apolipoprotein B (ApoB) and VLDL cholesterol. The impaired ability of insulin to inhibit free fatty-acid release leads to enhanced hepatic VLDL cholesterol production, which correlates with the degree of hepatic fat accumulation
2.1.1.2.1.1 The increased number of VLDL cholesterol particles and increased plasma triglyceride levels decrease the level of HDL and increase the conc of LDL via several processes
2.1.1.2.1.1.1 In these patients, inability of insulin to upregulate the ApoA-I production (owing to insulin resistance) might contribute to low HDL cholesterol levels
2.1.1.2.1.1.1.1 insulin resistance and low HDL levels might have a common mediator; for example, TNF. TNF is implicated in obesity-related insulin resistance and is known to lower serum HDL cholesterol levels
2.1.1.2.1.1.1.1.1 The dysregulation of the insulin receptor or IRS constitutes a common feature of insulin resistance. Mechanisms for this dysregulation might include tumor necrosis factor a (TNFa)-mediated downregulation of mRNA transcription
3 interventions
3.1 Exercise can also improve insulin sensitivity (independently of weight loss) and increases HDL cholesterol levels, especially in people with a high baseline HDL level
4 consequences of insulin resistance
4.1 Impairs insulin secretion in pancreas
4.2 insulin normally inhibits TAG breakdown. insulin resistance increase lypolysis and leads to hyperlipidemia causin dyslipidemia
4.2.1 increase circulating fatty acids leads to an increase in VLDL production by the liver resulting in an increase in circulating LDL levels
4.3 in the liver, gluconeogenisis and glycogenolysisi increases= hyperglycemia
4.4 reduces uptake of glucose by skeletal muscles. contributes to hyperglycemia
4.5 Differentiation of adipocytes is impaired. leads to hyperlipidemia
4.6 on its own does'nt cause T2D if b-cell can compensate by raising insulin secretion
5 insulin resistance
6 pathogenesis
6.1 impaired insulin secretion
6.1.1 b- cell dysfunction and death
6.1.1.1 ER stress
6.1.1.2 Glucotoxicity
6.1.1.2.1 Expression of many genes important for glucose-induced insulin release decreased progressively with increasing hyperglycemia, in parallel with a reduction of several islet transcription factors involved in β cell development and differentiation.
6.1.1.3 lipotoxicity
6.1.1.3.1 metabolic products from the excess fatty acids such as ceramides and precursors for oxidative stress induce beta-cell dysfunction and death
6.1.1.3.2 oxidative stress
6.2 insulin resistance
6.2.1 inflammation
6.2.2 glucotoxicity
6.2.3 Lipotoxicity
6.3 genetic/epigenetic factors
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