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IP3 diabetes > diabetes > Flashcards

diabetes Flashcards

1
Q

Define type 1 diabetes

A

Autoimmune disorder resulting in destruction of beta cells of the pancreas

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2
Q

Define type 2 diabetes

A

muscle cells, liver, and fat cells become insulin resistant and over time insulin production can decrease

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3
Q

What are the symptoms that can be seen at diagnosis of type 1 diabetes

A

the three P’s: polyuria, polydipsia, polyphagia

noctura and weight loss

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4
Q

What are the symptoms seen at diagnosis of type 2 diabetes

A

symptoms are not normally seen but you can see lethargy, polyuria, polydipsia, and noctura

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5
Q

What are the micro and macrovascular complications seen at time of diagnosis of type 1 DM

A

normally none

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6
Q

Do you see micro and macrovascular complications at time of diagnosis is type 2 DM

A

yes

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7
Q

what are the macrovascular complications of DM

A

arteriosclerotic and atherosclerotic events, coronary heart disease, cerebral vascular disease, peripheral arterial disease

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8
Q

what are the microvascular complications of DM

A

nephropathy, retinopathy, autonomic neuropathy, peripheral neuropathy

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9
Q

what are the prevalence’s of the different types of DM?

A

Type 1 DM accounts for 5-10% of all DM cases, type 2 accounts for 90%
10% of people greater than 20 have type 2 DM and it is more common in women

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10
Q

what populations are at greatest risk for type 2 DM

A

African Americans, Latinos, Native Americans, Asian Americans, Pacific Islanders

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11
Q

During what state do you see high glucagon and low insulin levels and what main processes are occuring

A

fasting state; gluconeogenesis, glycogenolysis, lipolysis, fatty acid oxidation, proteolysis, ketone body formation (starved state)

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12
Q

During what state do you see increased insulin levels and decreased glucagon levels, what main processes are occurring

A

fed state; glucose uptake, glycolysis, glycogenesis, fatty acid synthesis, lipogenesis,

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13
Q

what is the exocrine function of the pancreas

A

organized into a network of ducts surrounded by ductal cells that produce bicarbonate (to neutralize the acidic chyme that is expelled as the stomach empties into the duodenum), and acinar cells that produce digestive enzymes such as proteases, lipases, and amylases. These secretions collect in the pancreatic duct and are released into the intestinal lumen together as “pancreatic juice”

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14
Q

what is the endorcrine function of the pancreas

A

cluster in groups called the islets of Langerhans. These clusters contain five distinct cell types; α, β, δ, PP, and ε, which produce polypeptide hormones that are released into adjacent capillaries in response to various stimuli.

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15
Q

what are the pancreatic islet cells

A

two major subsets of hormone-producing cells, the glucagon-producing α-cells and insulin-synthesizing β-cells. There are more β-cells than α-cells

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16
Q

describe the islets of Langerhans

A

five distinct cell types; α, β, δ, PP, and ε, which produce polypeptide hormones that are released into adjacent capillaries in response to various stimuli.

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17
Q

describe the acinar cells

A

produce digestive enzymes such as proteases, lipases, and amylases that are released into the intestinal lumen with bicarbonate

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18
Q

describe the pancreatic duct

A

where bicarbonate and digestive enzymes from the acinar cells collect before dumping into the intestines

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19
Q

what is the primary stimulus for insulin release and what are the steps of its release

A

glucose is main stimulus

steps: 1) High blood glucose levels increase glucose transport into beta cells via the GLUT-2 transporter
2) Glucose is metabolized via glycolysis, creating ATP so ATP/ADP ratio increases
3) increased ATP/ADP ratio inhibits the ATP sensitive K channel causing the cell to depolarize and Ca to move in through the Ca channel
4) Immediate release of insulin; increased intracellular Ca levels stimulate release of insulin granules
5) if glucose remains high then insulin is actively synthesized

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20
Q

what other things cause insulin to be released other than glucose

A

increased plasma amino acid content, CCK, GIP, and GLP-1

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21
Q

describe insulin synthesis

A

Preproinsulin undergoes proteolytic cleavage in the RER to generate mature insulin and a cleavage peptide, C-peptide. (both are exocytosed) C peptide has longer half life

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22
Q

describe the insulin signaling pathway

A

Insulin binds IR (tyrosine kinase receptor) found on most tissues including liver, muscle, adipose. autophosphorylation of IR causes an increase in GLUT-4 transporters to be inserted into membrane of the cell, increase glycogenesis, lipogenesis, proteogenesis, stimulates cell growth and differentiation, and decreases lipolysis,

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23
Q

Which GLUT receptor is insulin dependent and which is insulin independent

A

GLUT 2 is insulin independent and GLUT 4 is insulin dependent

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24
Q

what is epinephrine’s effect on beta cells?

A

epeniephrine binds alpha adrenergic receptors on beta cells and inhibits release of insulin

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25
Q

what 3 main things stimulate glucagon secretion

A

decreased circulating glucose, increased plasma amino acid contents, increased circulating epinephrine

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26
Q

how is glucagon synthesized

A

large, inactive prohormone peptide. The glucagon polypeptide becomes activated by post-translational cleavage and is secreted from α-cells into the circulation.

27
Q

describe the glucagon signaling pathway

A

glucagon binds glucagon receptor (G coupled protein receptor), stimulates Gs which stimulates adenylyl cyclase (AC) which catalyzes formation of cAMP which activates cAMP-dependent protein kinase (PKA) which phosphorylates serine or threonine residues leading to changes on the metabolic output of the liver (increases glycogenolysis, gluconeogenesis, and uptake of amino acids in the liver, and release of fatty acids from adipose tissue)

28
Q

describe amylin

A

37-residue peptide hormone that is co-secreted from the pancreas with insulin in a ratio of approximately 1:100, amylin:insulin. amylin is synthesized in β-cells as an inactive prohormone precursor. undergoes post-translational cleavage and modification in the cell prior to secretion. It suppresses glucagon release, slows gastric emptying, satiety factor

29
Q

Describe the role of renal sodium-glucose cotransporters in glucose homeostasis

A

SGLT1 and SGLT2 are expressed in the distal proximal convoluted tubule, SGLT2 accounts for 90% of renally absorbed glucose, and SGLT1 10%. When they are saturated like in times of hyperglycemia then glucose excretion is increased

30
Q

explain the biological role of GLP-1 and GIP

A

GLP-1 is encoded on the same gene as glucagon, its released from intestinal L cells and induces insulin secretion when blood glucose levels are greater than 90, also a satiety factor
GIP is secreted by intestinal K cells, induces insulin secretion.

31
Q

what does DPP-4 do?

A

cleaves GLP-1 and GIP so they can’t induce insulin secretion

32
Q

describe glucose absorption, digestion, and transport

A

complex carbohydrates are broken down to di and mono sacchrides which are then absorbed into the blood stream to go to either the liver or peripheral tissues. There they are broken down for energy or stored

33
Q

What role does glycolysis play in cellular respiration

A

It is the first step of respiration that breaks glucose down to pyruvic acid

34
Q

what are the role of proteins in cellular respiration

A

they are broken down to amino acids that can feed into glycolysis or the krebs cycle, or made into proteins or nitrogen

35
Q

what are the roles of fats in cellular respirations

A

broken down to glycerol and fatty acids, glycerol can be fed into glycolysis or stored as fat and fatty acids can become acetyl coA or become fat

36
Q

what are the metabolic pathways involving glucose

A

glycolysis, glycogenesis, glycogenolysis, gluconeogenesis, or fed into the pentose phosphate pathway when glucose becomes g-6-P

37
Q

what is G-6-P involved in

A

continue glycolysis, go into pentose phosphate pathway, end product of gluconeogenesis, substrate for glycogen formation, and its end product

38
Q

describe hexokinases role and its vmax, km, and when/where it works, what inhibits it

A

phosphorylizes glucose in most cells, has a lower vmax than glucokinase and a lower km, it works in lower glucose levels than glucokinase and it’s inhibited by G-6-P

39
Q

describe glucokinase

A

higher vmax and km than hexokinase, found in liver cells and pancreatic islet cells, exhibits cooperativity, (0-1 is negative, 1+ is positive and in the middle of the s curve where glucokinase is most sensitive to glucose. glucokinase helps prevent hyperglycemia.

40
Q

What affect would a decrease in glucokinase have

A

it would decrease glycogen production in liver cells, and decrease phosphorylation of glucose in beta cells thus decreasing the sensitivity of beta cells to glucose

41
Q

what affect would a decrease in hexokinase have

A

decrease glycolysis, glycogen formation, and lipid formation

42
Q

glycolysis highlights

A

rate limiting step is formation of fructose 1,6-bisphosphate from fructose-6-phosphate by phosphofrutokinase-1 (PFK-1), 4 atp made, 2 used, ends with two molecules of pyruvate, 2 NADH’s are made. pyruvate is converted into acetyl coA by pyruvate dehydrogenase in he mitochondria

43
Q

what does PFK-1 do

A

phosphorylates fuctose-6-phosphate to fructose-1.6-bisphosphate in glycolysis

44
Q

what does pyruvate kinase do

A

converts phosphoenalpyruvate to pyruvate at the end of glycolysis

45
Q

what does pyruvate dehydrogenase do

A

in the mitochondria converts pyruvate to acetyl coA

46
Q

TCA cycle and oxidative phosphorylation

A

TCA cycle produces CO2 and substrates for oxidative phosphorylation via oxidation reactions
Oxidative phosphorylation creates the most amount of ATP

47
Q

what does glucose-6-phosphotase do and what cells express it

A

converts G-6-P to glucose, only liver

48
Q

describe gluconeogenesis and where it occurs

A

kidneys and liver, non carbohydrate precursors (glycerol, amino acids), pyruvate carboxylase converts pyruvate to oxaloacitate, phosphoenolpyruvate carboxylkinase converts (PEPCK) oxaloacitate to phosphoenolpyruvate, fructoes-bisphosphatase-1 makes fructose-6-phosphate, glucose-6-phosphotase make glucose

49
Q

what pathway is pyruvate carboxylase part of

A

gluconeogenesis

50
Q

what pathway is PEPCK park of

A

gluconeogenesis

51
Q

what pathway is fructose-6-bisphosphatase-1 part of

A

gluconeogenesis

52
Q

what pathway is glucose-6-phosphotase part of

A

gluconeogenesis

53
Q

what does the pentose phosphate pathway do

A

(also known as the hexose monophosphate shunt) produces the 5-carbon sugar ribose, which is necessary for de novo synthesis of nucleic acids, from G6P. This pathway also generates the reduced form of NADPH, and is critical to many anabolic pathways which require that molecule as a reducing agent

54
Q

discuss fructose-1,2-bisphosphates allosteric interactions

A

allosterically inhibits fructose bisphosphotase -1 and activate PFK-1

55
Q

what allosterically activates pyruvate carboxylase?

A

acetyl coA

56
Q

what happens in the liver during the fed state

A

glycolysis, glycogenosis, fatty acid synthesis

57
Q

what happens in the adipose tissue during fed state

A

glycolysis, lipogenesis

58
Q

what happens in muscle tissue during fed state

A

glycolysis, glycogenosis

59
Q

what happens in muscle during fasting

A

glycogenolysis, fatty acid oxidation, proteolysis

60
Q

ketogenesis

A

excess acetyl CoA is generated and, subsequently converted to acetoacetate, β-hydroxbutyrate, and acetone, ketone bodies are converted back to acetyl coA in cells to be used

61
Q

pathophysiology of type 1 DM

A

clinical symptoms appear once 80-90% of the beta cells are destroyed due to T cell mutations or viral infections , can lead to hyperlipidemia

62
Q

pathophysiology of type 2 DM

A

begins when insulin resistance is accompanied by beta cell impairment,
central obesisty if main cause of insulin resistance and TG over 150, and leptin, resistin, and adiponectin

63
Q

describe the effects of leptin, FGF21, and adiponectin

A

adiponectin is decreased in people with insulin resistance, regulates glucose and fatty acid metabolism via AMPK, leptin is a satiety factor and stimulates energy expenditure, increase leptin with increased obesity, FGF21 increased GLUT1 in adipocytes, regulates glucose homeostatis and lipid metabolism, increased in obese, type 2, and insulin resistant, decreases glucagon secretion

IP3 diabetes (2 decks)

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