Energy Metabolism - Diabetes Mellitus & Obesity Flashcards

1
Q

Key biochemical events that underlie the responses of muscle to insulin

A

glucose uptake

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2
Q

Key biochemical events that underlie the responses of adipocytes to insulin

A
  • Stimulate lipoprotein lipase to facility break down of lipids which carry fats into blood stream so more can be taken up by adiposcyte
  • Glucose and FA are made into triglycerides within the lipocyte
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3
Q

Key biochemical events that underlie the responses of liver cells to insulin

A
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4
Q

What protein does insulin stilumate for glucose uptake?

A

Insulin-stimulated GLUT4 translocation leads to glucose uptake by muscle and adipose cells.

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5
Q

Diabetic ketoacidosis cause

A

develops when your body doesn’t have enough insulin to allow blood sugar into your cells for use as energy.

  • catabolic processes prevail
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6
Q

Key characterisitics of diabetic ketoacidosis

A
  • Urinary excretion of glucose and ketones
    • frequent urination and thirs
  • Osmotic diuresis
  • Plasma acidosis
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7
Q

What two ketones contribute to diabetic ketoacidosis?

A

Two ketones produced by the liver include acetoacetate (first ketone made in fasting state) as well as beta hydroxy butyrate. The acid of these ketones can dissociate to produce H+ and leads to acidosis. Excessive ketones leads to more acidic plasma

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8
Q

Hallmarks of diabetes mellitus

A
  1. high blood glucose (hyperglycemia) levels when uncontrolled
  2. relative insulin deficiency
    1. True for type I (absolute not produced) and type II (still produces insulin but defective pathway so pancreas may try to make more but still not enough for metabolic actions)
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9
Q

Type 1 diabetes

A

(insulin-dependent / “juvenile” DM)

  • 10% of all diabetic subjects
  • Insulin secretion reduced or absent
    • Result of autoimmune disorder body fails to recognize beta pancreatic cells as itself and immune response to attack and destroy them
  • Treated by insulin injections or insulin pumps
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10
Q

Type II diabetes

A

(non-insulin-dependent / “mature-onset” DM)

  • 90% of all diabetic subjects
  • Target cell responsiveness to insulin is reduced, and defect in insulin secretion
  • Treated by diet, exercise, oral medications (e.g. metformin, sulfonylureas), GLP-1 agonists, sometimes insulin injections.
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11
Q

Why is target cell responsiveness of type II diabetes reduced?

A

Body thinks it doesn’t see the metabolic action so it makes more to see if it respond and initially it works but over time it is not sufficient and pancreas tires out anf fails to continue to work hard and get beta cell failure. Often people with type II have more insulin but just not working

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12
Q

Overweight

A

The clinical definition of overweight is a functional one, a state in which an increased amount of fat in the body results in a significant impairment of health from a variety of diseases and disorders – notably, hypertension, atherosclerosis, heart disease, diabetes, and sleep apnea.

  • ~ ¼ Canadians are obese
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13
Q

Obesity

A

Obesity denotes a particularly large accumulation of fat – that is, extreme overweight.

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14
Q

prevalance of diabetes mellitus

A

1/3 Canadians have type I or type II

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15
Q

Brains role in the control of food intake

A

Picks up signals from peripheral and external environment and tells us when to find food and when to stop. Hypothalamus is important as it interacts with other brain regions to for food uptake.

  • Brain has mechanisms that can sense nutrients and hormones
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16
Q

Stimulations and suppressions of of the control of food intake

A
17
Q

Role of energy in controlling energy stores

A

Potent satiety hormone - discovered in mid 19990s.
Secreted by fat tissue. Signal of adiposity and tells brain fat stores are plentiful and we don’t need to keep eating. As such compared to GI hormones insulin it is more a long term satiety signal.

  • modulates neural circuits that body has adequate nutrient supply
18
Q

Negative feedback for lepton secretion

A

decreased energy intake and increased metabolic rate turns off further lepton secretion

19
Q

Lepton resistance

A

brain becmoes insensitive to lepton - increase in lepton fails to signal satiety and even though ample ft stores hunger is not suppressed. Leptin resistance can occur in brain and can contiribute to obesity

20
Q

Hypoglycemia in diabetes

A

low blood sugar

  • can be fatal
  • bed and dead syndrome → low blood sugar while sleeping and don’t know it
21
Q

normal counterregulation to hypoglycemia

A
  • decreased insulin secretion from beta cells
  • increased glucagon from alpha cells and potent activator of glucose
  • increased secretion of epi from adrenal medulla
    • stress hormone increased glucose levels
  • increased cortisol from adrenal cortex
    • stress hormone increases glucose levels
22
Q

Sympathetic response to low plasma glucose

A
23
Q

Long-term complications of diabetes mellitus

A

Large vessel disease

  • Stroke
  • Heart attack
  • Heart failure

Small vessel disease: blood vessel weakening and breakage

  • Nephropathy
  • Retinopathy
  • Neuropathy