724129
Description
Mind Map by fatimaelfitouri, updated more than 1 year ago
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Created by fatimaelfitouri
over 10 years ago
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T2D
- insulin
- how does insulin affect metabolic pathways and how it influences energy balance
- glucagon as anatagonist effects to insulin
- 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
- Insulin is the principal hormone that regulates uptake of glucose
from the blood into most cells, including skeletal muscle cells and
adipocytes.
- Insulin is also the major signal for conversion of glucose
to glycogen for internal storage in liver and skeletal muscle
cells
- Insulin has autacoid (stimulatory) and chalone (inhibitory) actions
- Insulin promotes glucose uptake by stimulating the translocation of
GLUT4 from intracellular sites
- increases the activity of several enzymes in the glycolytic
pathway including glucokinase
- Insulin does not stimulate glucose uptake in the liver, it inhibits
glycogenolysis and gluconeogenesis
- Insulin up regulates transcription of
PFK, PK and PDH
- Differentiation of adipocytes is insulin dependent
- Insulin inhibits HSL (hormone sensitive
lipase). HSL breaks down TG to FA
- how does insulin affect metabolic pathways and how it influences energy balance
- common features
- impaired glucose handing caused by dyslipidemia
- Dyslipidemia
- characteristic features of this phenotype are a high plasma
triglyceride concentration, low HDL cholesterol concentration
and increased concentration of small dense LDL–cholesterol
particles.
- the prevalence of high plasma triglyceride and low HDLs levels in individuals with diabetes mellitus is
significantly higher than in those without diabetes mellitus
- the prevalence of high plasma triglyceride and low HDLs levels in individuals with diabetes mellitus is
significantly higher than in those without diabetes mellitus
- 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
- 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
- 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
- In these patients, inability of insulin to upregulate the ApoA-I production (owing to insulin resistance) might
contribute to low HDL cholesterol levels
- 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
- 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
- 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
- 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
- In these patients, inability of insulin to upregulate the ApoA-I production (owing to insulin resistance) might
contribute to low HDL cholesterol levels
- 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
- 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
- characteristic features of this phenotype are a high plasma
triglyceride concentration, low HDL cholesterol concentration
and increased concentration of small dense LDL–cholesterol
particles.
- Dyslipidemia
- impaired glucose handing caused by dyslipidemia
- interventions
- Exercise can also improve insulin sensitivity (independently of weight loss) and increases HDL cholesterol levels,
especially in people with a high baseline HDL level
- Exercise can also improve insulin sensitivity (independently of weight loss) and increases HDL cholesterol levels,
especially in people with a high baseline HDL level
- consequences of insulin resistance
- Impairs insulin secretion in
pancreas
- insulin normally inhibits TAG breakdown. insulin resistance increase lypolysis
and leads to hyperlipidemia causin dyslipidemia
- increase circulating fatty acids leads to an increase in VLDL production
by the liver resulting in an increase in circulating LDL levels
- increase circulating fatty acids leads to an increase in VLDL production
by the liver resulting in an increase in circulating LDL levels
- in the liver, gluconeogenisis and glycogenolysisi increases= hyperglycemia
- reduces uptake of glucose by skeletal
muscles. contributes to hyperglycemia
- Differentiation of adipocytes is impaired. leads to hyperlipidemia
- on its own does'nt cause T2D if b-cell can
compensate by raising insulin secretion
- Impairs insulin secretion in
pancreas
- insulin resistance
- pathogenesis
- impaired insulin secretion
- b- cell dysfunction and death
- ER stress
- Glucotoxicity
- 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.
- 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.
- lipotoxicity
- metabolic products from the excess fatty acids such as ceramides and
precursors for oxidative stress induce beta-cell dysfunction and death
- oxidative stress
- metabolic products from the excess fatty acids such as ceramides and
precursors for oxidative stress induce beta-cell dysfunction and death
- ER stress
- b- cell dysfunction and death
- insulin resistance
- inflammation
- glucotoxicity
- Lipotoxicity
- inflammation
- genetic/epigenetic factors
- impaired insulin secretion
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