normal glucose homeostasis
Glucose production in the liver
Glucose uptake and utilization by peripheral tissues (skeletal muscle)
Actions of hormones
normal glucose levels:
70-120mg/dl
FXN of insulin
to increase the rate of glucose transport into certain cells of the body
gluconeogensis
formation of glucose from excess amino acids, fat, and other non carbohydrate sources.
glycogenesis
formation of glycogen
lipogenesis
formation of fats
glycogenolysis
process that coverts glycogen to glucose
glycolysis
hydrolysis of glucose to pyruvate
lipolysis
catabolic degradation of triacylglycerol
pancreas general info list
Exocrine
Endocrine
Islets
Alpha Cells --> glucagon
Beta Cells --> proinsulin
Delta Cells --> somatostatin (suppress insulin and glucagon)
F cells --> Pancreatic Polypeptide (PP) cells
Epsilon Cells make gherlin, which causes hunger
insulin:fats
In-creased glucose uptake
-in-creased lipogenesis
-de-creased lipolysis
insulin:muscle
in-creased glucose uptake
in-creased glycogen synthesis
in-creased protein synthesis
insulin:liver
de-creased gluconeogenesis
in-creased glycogen synthesis
in-creased lipogenesis
glucose-dependent insulinotropic polypeptide (GIP)
glucagon-like peptide 1 (GLP-1)
the ingestion of nutrients causes to release these hormones from the cell in the gut.
they stimulate the production of insulin and inhibit glucagon
insulin increases or decreases glucose?
decreases
glucagon increases or decreases glucose?
increases
cortisol and adrenal corticosteroids decrease or increase glucose?
increases
epinephrine increases or decreases glucose?
increases
GH increases or decreases gluose?
increases
Thyroxine increases or decreases glucose?
increases
somatostatin increases or decreases glucose?
inhibits insulin and glucagon
gastric inhibitory peptide increases or decreases glucose?
stimulates insulin release
...
...
metabolic action of insulin
Fed state
glucose provides primary energy source amylin on area postrema ( AP)
INSULIN dominates!
fasting state
glucose is produced by glycogenolysis and gluconeogenesis
GLUCAGON dominates!
regulation of glucose metabolism
EXERCISE
Initially insulin levels drop and glucagon and catecholamine levels rise
STRESS
Production of stress hormones (corticosteroids and catecholamines) increase production of glucose
Increase production of FFAs
Lead to hyperglycemia
diabetes meellitus means_____ intolerance
glucose
how do you diagnose DM?
More than one fasting plasma glucose level (>126)
Elevated plasma glucose in response to an oral glucose tolerance test (>200)
Polydipsia, polyphagia, polyuria
...
type 1 diabetes characteristics
Genetic
Autoimmune
Childhood (juvenile) onset
Antibodies to beta cells, insulitis
Beta cell depletion
NON-OBESE patients
type 2 diabetes characteristics
Genetic, but diff. from Type 1
NOT autoimmune
Adult, or maturity onset, e.g., 40's, 50's
Insulin may be low, BUT, peripheral resistance to insulin is the main factor
OBESE patients
what is MODY?
the 3rd diabetes
the mature onset diabetes of the young.
an inheritance of defected b cells
classifcation of diabetes mellitus
gestational is important to monitor
...
HLA's
expression of certain HLAs is associated with increased susceptibility to type I diabetes.
Viruses
are considered initiating factors in autoimmune cause of type I diabetes.
insulin receptors defects
Insulin resistant: can be due to malfunction in insulin receptor, but the cause is not known. In type II diabetes.
Antibodies to insulin receptor: in type II diabetes.
glucose transport
: low levels of glucose transporters in type I and II diabetes.
pathogenesis of type 1 DM
caused by destruction of islet cells as a result of autoimmune reaction to -cells.
pathogenesis of type 2 DM
caused by a defect in glucose transport after insulin binds to its receptor.
complications of type 1 DM
NeuropathY--> type 1 diabetes are at risk earlier at life
Type 1 diabetes treatmenT--> insulin treatment
Pancrease gets burnt out-->diabetes type 2 will get insulin shots like diabetes 1
complications type 1 DM
Genetic susceptibility
Environmental factors
Immunologically mediated destruction of beta cells
Peak about 10-14 years of age
A 12-year-old female is newly diagnosed with type 1 diabetes mellitus (DM). Which of the following is the most likely cause of her disease?
A. A familial, autosomal dominant gene defect
B. Obesity and lack of exercise
C. Immune destruction of the pancreas
D. Hyperglycemia from eating too many sweets
C
metabolic acidosis in type 1 DM
ketoacidosis occurs primarily in type 1 DM as a result of increased lipolysis and conversion to ketone bodies. excessive ketone bodies accounts for metabolic acidosis, which is reckonized by a fall in pH ans bicarbonate levels.
type 2 DM
resistant to the action of insulin
risk factors:: high BMI (intra-abdominal obesity), family history of DM2, ethnic minority, female gender
Insulin is less able to facilitate entry of glucose into live, skeletal muscles, adipose tissue
Pancreas eventually "burns out"
Insulin is less able to facilitate entry of glucose into live, skeletal muscles, adipose tissue
Pancreas eventually "burns out
pathogenesis type 2 DM
Hyperglycemia in type 2 diabetes mellitus is a result of:
A. insulin deficiency.
B. hyperinsulinemia and insulin resistance.
C. glucagon deficiency.
D. liver dysfunction.
B
normal glucose homeostasis
Glucose production in the liver
Glucose uptake and utilization by peripheral tissues (skeletal muscle)
Actions of hormones
normal glucose levels:
70-120mg/dl
FXN of insulin
to increase the rate of glucose transport into certain cells of the body
gluconeogensis
formation of glucose from excess amino acids, fat, and other non carbohydrate sources.
glycogenesis
formation of glycogen
lipogenesis
formation of fats
glycogenolysis
process that coverts glycogen to glucose
glycolysis
hydrolysis of glucose to pyruvate
lipolysis
catabolic degradation of triacylglycerol
pancreas general info list
Exocrine
Endocrine
Islets
Alpha Cells --> glucagon
Beta Cells --> proinsulin
Delta Cells --> somatostatin (suppress insulin and glucagon)
F cells --> Pancreatic Polypeptide (PP) cells
Epsilon Cells make gherlin, which causes hunger
insulin:fats
In-creased glucose uptake
-in-creased lipogenesis
-de-creased lipolysis
insulin:muscle
in-creased glucose uptake
in-creased glycogen synthesis
in-creased protein synthesis
insulin:liver
de-creased gluconeogenesis
in-creased glycogen synthesis
in-creased lipogenesis
glucose-dependent insulinotropic polypeptide (GIP)
glucagon-like peptide 1 (GLP-1)
the ingestion of nutrients causes to release these hormones from the cell in the gut.
they stimulate the production of insulin and inhibit glucagon
insulin increases or decreases glucose?
decreases
glucagon increases or decreases glucose?
increases
cortisol and adrenal corticosteroids decrease or increase glucose?
increases
epinephrine increases or decreases glucose?
increases
GH increases or decreases gluose?
increases
Thyroxine increases or decreases glucose?
increases
somatostatin increases or decreases glucose?
inhibits insulin and glucagon
gastric inhibitory peptide increases or decreases glucose?
stimulates insulin release
...
...
metabolic action of insulin
Fed state
glucose provides primary energy source amylin on area postrema ( AP)
INSULIN dominates!
fasting state
glucose is produced by glycogenolysis and gluconeogenesis
GLUCAGON dominates!
regulation of glucose metabolism
EXERCISE
Initially insulin levels drop and glucagon and catecholamine levels rise
STRESS
Production of stress hormones (corticosteroids and catecholamines) increase production of glucose
Increase production of FFAs
Lead to hyperglycemia
diabetes meellitus means_____ intolerance
glucose
how do you diagnose DM?
More than one fasting plasma glucose level (>126)
Elevated plasma glucose in response to an oral glucose tolerance test (>200)
Polydipsia, polyphagia, polyuria
...
type 1 diabetes characteristics
Genetic
Autoimmune
Childhood (juvenile) onset
Antibodies to beta cells, insulitis
Beta cell depletion
NON-OBESE patients
type 2 diabetes characteristics
Genetic, but diff. from Type 1
NOT autoimmune
Adult, or maturity onset, e.g., 40's, 50's
Insulin may be low, BUT, peripheral resistance to insulin is the main factor
OBESE patients
what is MODY?
the 3rd diabetes
the mature onset diabetes of the young.
an inheritance of defected b cells
classifcation of diabetes mellitus
gestational is important to monitor
...
HLA's
expression of certain HLAs is associated with increased susceptibility to type I diabetes.
Viruses
are considered initiating factors in autoimmune cause of type I diabetes.
insulin receptors defects
Insulin resistant: can be due to malfunction in insulin receptor, but the cause is not known. In type II diabetes.
Antibodies to insulin receptor: in type II diabetes.
glucose transport
: low levels of glucose transporters in type I and II diabetes.
pathogenesis of type 1 DM
caused by destruction of islet cells as a result of autoimmune reaction to -cells.
pathogenesis of type 2 DM
caused by a defect in glucose transport after insulin binds to its receptor.
complications of type 1 DM
NeuropathY--> type 1 diabetes are at risk earlier at life
Type 1 diabetes treatmenT--> insulin treatment
Pancrease gets burnt out-->diabetes type 2 will get insulin shots like diabetes 1
complications type 1 DM
Genetic susceptibility
Environmental factors
Immunologically mediated destruction of beta cells
Peak about 10-14 years of age
A 12-year-old female is newly diagnosed with type 1 diabetes mellitus (DM). Which of the following is the most likely cause of her disease?
A. A familial, autosomal dominant gene defect
B. Obesity and lack of exercise
C. Immune destruction of the pancreas
D. Hyperglycemia from eating too many sweets
C
metabolic acidosis in type 1 DM
ketoacidosis occurs primarily in type 1 DM as a result of increased lipolysis and conversion to ketone bodies. excessive ketone bodies accounts for metabolic acidosis, which is reckonized by a fall in pH ans bicarbonate levels.
type 2 DM
resistant to the action of insulin
risk factors:: high BMI (intra-abdominal obesity), family history of DM2, ethnic minority, female gender
Insulin is less able to facilitate entry of glucose into live, skeletal muscles, adipose tissue
Pancreas eventually "burns out"
Insulin is less able to facilitate entry of glucose into live, skeletal muscles, adipose tissue
Pancreas eventually "burns out
pathogenesis type 2 DM
Hyperglycemia in type 2 diabetes mellitus is a result of:
A. insulin deficiency.
B. hyperinsulinemia and insulin resistance.
C. glucagon deficiency.
D. liver dysfunction.
B