Introduction to diabetes Flashcards

1
Q

where is insulin produced?

A
Endocrine gland of the Pancreas by beta cells
the endocrine gland also secretes:
-glucagon (alpha cells)
-somatostatin (SS) (delta cells)
-Pancreatic polypeptide (PP)
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2
Q

What is insulin?

A

an anabolic hormone

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3
Q

what is the role of insulin in the body?

A

Signals liver, muscle and fat cells to take in glucose from the blood
Sufficient energy – liver stores glucose as glycogen
Promotes storage of carbohydrate and fat and protein synthesis

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4
Q

How is insulin produced?

A
  • mRNA transcript is translated into an inactive protein – preproinsulin
  • Contains an amino-terminal signal sequence that is required to pass through ER membrane
  • Post-translational processing removes un-needed portions
  • Preproinsulin enters ER and rendered useless, is proteolytically removed to form proinsulin
  • Post-translational modification and cleavage to form insulin
  • Insulin packaged and stored in secretory granules which accumulate in the cytoplasm until release is triggered
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5
Q

How is insulin released?

A

(BIPHASIC RESPONSE)

  • Glucose entry in to beta cells via GLUT2 transporters
  • Glycolysis → ATP
  • ↑ATP:ADP → depolarisation
  • Opening to Ca2+ channels
  • Ca2+ influx triggers exocytosis of insulin-storing granules
  • Diffusion of insulin in to nearby blood vessels
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6
Q

define diabetes mellitus

A

metabolic condition that is characterised by chronic hyperglycaemia: diabetes (‘siphon’) mellitus (‘sweet’)

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7
Q

Outline Type 1 diabetes

A
  • Insulin-dependent diabetes mellitus (IDDM); juvenile onset
  • Destruction of pancreatic beta cells in the islets of Langerhans by the body’s own white blood cells (T cells); autoimmune disease
  • Pancreas cannot produce insulin
  • Regular insulin injections
  • 5-10% of all diabetes
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8
Q

Outline Type 2 diabetes

A
  • Non-insulin-dependent diabetes mellitus (NIDDM)
  • Variable degrees of insulin resistance, impaired insulin secretion and increased glucose production
  • can be controlled through diet, exercise and weight loss
  • Others require oral medications and/or insulin
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9
Q

Risk factors for diabetes

A
mix of genes and enviroment
some say rise in type 2 is all down to enviroment.
eg.:
Age
Obesity
Physical inactivity
High blood pressure
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10
Q

what charachterises type 2 diabetes?

A

insulin resistance- less glucose in a given amount of blood compared to a control
Obesity may desensitise muscle and fat cells to effects of insulin
↓GLUT-4 translocation

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11
Q

identify the 4 recent hypothesis used to explain type 1 diabetes

A

sunshine hypothesis- ziptis and akobeng 2008
cows milk hypothesis- knip et al. 2014
hygeine hypothesis- okada et al. 2010
accelerator hypothesis- wilkin et al. 2001

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12
Q

what are the main symptoms of diabetes?

A
Polydipsia (extreme thirst)
Polyuria (increased urine volume and 
Increased hunger
Unexplained weight loss
Extreme tiredness
Blurred vision
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13
Q

what is retinopathy and what are the symptoms

A

(diabetic) retinopathy occurs in the eyes.
capillaries around retina blocked
blurred vision/blindness

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14
Q

what is nephropathy and what are the symptoms

A

occurs in the kidneys
fluid/waste retention
results in increased BP and kidney failure

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15
Q

what is Diabetic ketoacidosis

A
breakdown of body tissue
causes: 
High blood glucose
ketones in blood/urine
nausea
ketones in breath
unconciousness
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16
Q

What is GLUT-4?

A

GLUT4 is the insulin-regulated glucose transporter found primarily in adipose tissues and striated muscle (skeletal and cardiac).

Recent reports demonstrated the presence of GLUT4 gene in central nervous system such as the hippocampus and showed it was linked to changes in behaviour (induced depressive behaviour) and cognitive function

17
Q

what is AMPK and what role does it play in diabetes?

A

AMP-activated protein kinase
expressed in liver, brain and skeletal muscle
AMPK is produced during exercise:
-during muscle stimulation AMP increases as ATP decreased, AMP forms AMPK
-activated via upstream kinase comples AMPKK
-during exercise the muscle is under increased stress due to the need to more ATP
-AMPK increases cellular energy levels by inhibiting energy consuming pathways (fatty acid synthesis) and stimulating energy producing pathways ( i.e. GLUCOSE TRANSPORTATION, GLUT-4)

EXTRA INFO: RECENT RESEARCH HAS IMPLICATED EXCESS AMPK IN ALZHEIMERS