Pancreas Flashcards

1
Q

Human metabolic processes outside cell vs inside cell

A

Outside the cell:
Keep blood glucose levels within a constant range during the fed, fasted, and starved state.

  1. Inside the cell:
    Maintain intra-cellular ATP and provide energy for high energy requiring tissues and anabolic processes
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2
Q

Normal fasting BG: 70-100 mg/dl

Normal BG 2h after meal:

A

Normal fasting BG: 70-100 mg/dl

Normal BG 2h after meal: <139 mg/dl

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3
Q

Blood glucose is kept within a narrow range via

A

Blood glucose is kept within a narrow range via tight hormonal regulation

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4
Q

glucose pathway after a meal

A
  1. glucose enters blood through intestine
  2. insulin is secreted
  3. glucose uptake by liver, adipose , and skeletal m.
    `
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5
Q

explain cahilll diagram based on phases

A

When awake, we eat approx. every 4 hours. We keep ourselves in Phase I of the Cahill Diagram.

Glucose supply between 4 – 12 hours (i.e during the last half of nocturnal sleep) comes from glucose stored as glycogen from the liver (Phase II), Glycogenolysis.

Beyond 12 hours, glucose has to be newly made by mobilizing stored energy rich substrates. This occurs mainly in the liver (Phase III), Gluconeogenesis.

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6
Q

The main hormone regulating metabolism during fasting is

A

The main hormone regulating metabolism during fasting is Glucagon

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7
Q

Main energy carriers in nutrition

A

Carbohydrates: approx. 4.7 kcal/g, main source of nutritional energy
50% of all calories in diet

Lipids: approx. 9 kcal/g, 20-30% or all calories in diet

Proteins: approx. 4.7 kcal/g, 20-30% of all calories in diet

Nucleotides: have potential caloric value, but do not significantly contribute to energy (ATP) production.

Ethanol: approx. 7 kcal/g

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8
Q

Digestive phase: Metabolism orchestrated almost entirely by

A

Digestive phase: Metabolism orchestrated almost entirely byinsulin.

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9
Q

Fating phase metabolism is regulated by

A

Glucagonandcatecholamines(epinephrine, norepinephrine)

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10
Q

what two hormones PARTIALLY contribute to fasting phase/

A

Growth hormone and cortisol also contribute somewhat to fasting-phase metabolism.

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11
Q

alphas and beta cells of pancreas

A

Beta cells produce insulin which induces uptake of blood glucose

Alpha cells produce glucagon (counter-regulation) which induces gluconeogenesis and glycogenolysis, leading to secretion of glucose and increase blood glucose

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12
Q

delta cells of pancreas

A

Delta cells produce somatostatin which inhibits the influx of glucose and amino acids; and decrease gastric secretion

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13
Q

insulin action in the liver

A

Insulin action promotes nutrient storage.
In the liver.
Insulin signaling through Akt2 activates glycogen synthase
decreases the transcription of gluconeogenic enzymes via inactivation of FOXO1.

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14
Q

Insulin effect on skeletal muscle,

A

In skeletal muscle, insulin activates glucose uptake and glycogen synthesis.

Skeletal muscle will also take up FAs for oxidation.

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15
Q

insulin effect on adipose tissue

A

In adipose tissue, insulin inhibits lipolysis & promotes glucose uptake.

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16
Q

type of glucose transpoters for skeletal muscle, adipose and liver

A

skel m and adipose are GLUT4- Need insulin to stimulate

liver is GLUT 2 which is on cell surface always taking in glucose

17
Q

Blood Perfusion of the Pancreatic Islets
A
B
D

A

75%
20%
5%

18
Q

Regulation of Insulin : β Cell Insulin Release PATHWAY

A
  1. entry of glucose into cell by GLUT 2
  2. Glucose is phosphorylated by glucokinase G6P
  3. metabolism of G6P by glycolysis, TCA and ox. phos
  4. K channel closes
  5. Depolarization of the cell6
  6. Ca influx in cell’
  7. GLP-1 Glucagon like peptide - induced PKA activates EXOCYTOSIS OF INSULIN
19
Q

Primary and secondary signals for insulin secretion

A

The main stimulus for beta cell secretion of insulin is elevated plasma glucose

Plasma amino acids as well as the elevation of parasympathetic activity and G.I. tract hormones, secondary to food intake, serve as secondary stimuli

20
Q

AkT role in mechanism of insulin

A
  1. translocate GLUT4 for glucose import
    AND
  2. INHIBIT FOX01- stop gluconeogenesis and VLDL Export
21
Q

insulin inhibits

A

GLYCOGEN BREAKDOWN
LIPOLYSIS (FAT BREAKDOWN)
PROTEIN BREAKDOWN

22
Q

glucagon inhibits

A

LIPID SYNTHESIS
PROTEIN SYNTHESIS
GLYCOGEN SYNTHESIS
DNA SYNTHESIS

23
Q

type 1 vs type 2 hyperglycemia

A

1) Type 1 which is secondary to low insulin secretion (autoimmune disease destruction of pancreatic beta cells),
(2) Type 2 which is associated with target tissue resistance to insulin (receptor or post-receptor defects)

24
Q

DM complications :Acute vs chronic

A

Acute (ketoacidosis & tissue dehydration)

Chronic (cardiovascular disease, blindness, renal failure, peripheral neuropathy, and impaired wound healing

25
Q

hypoglycemia

A

Caused by excess insulin, failure of the glucose counter-regulatory system or drugs

26
Q

types of symptoms of hypoglycemia

A

Neurogenic (autonomic)
Includes sweaty, hungry, tingling, shaky/tremelous, heart pounding or nervous/anxious feelings
Neuroglycopenic
Includes warm, weak, difficulty thinking/confused, tried/drowsy, faint, dizzy, difficulty speaking, blurred vision

27
Q

3) Maturity-onset Diabetes of the Young (MODY)

A

3) Maturity-onset Diabetes of the Young 3) Maturity-onset Diabetes of the Young (MODY) which is associated with defective insulin secretion by the pancreas (MODY) w

28
Q

hypoglycemia symptoms

A

Neurogenic (autonomic)
Includes sweaty, hungry, tingling, shaky/tremelous, heart pounding or nervous/anxious feelings

Neuroglycopenic
Includes warm, weak, difficulty thinking/confused, tried/drowsy, faint, dizzy, difficulty speaking, blurred vision

29
Q

type 1 symptoms

A

May present as chronic fasted state, “melting flesh”, ketosis, acidosis, glucosurea, diuresis & coma