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Biochemistry 2nd Year > Chp 36; Insulin Glucose Homeostasis And Diabetes Mellitus > Flashcards

Chp 36; Insulin Glucose Homeostasis And Diabetes Mellitus Flashcards

1
Q
  1. World diabetes day?
  2. 3rd leading cause of death?
  3. What is diabetes mellitus? Its types?
A
  1. 14th november
  2. Diabetes mellitus
  3. Diabetes mellitus is a group of metabolic disorders characterized by high blood sugar levels over a prolonged period. It occurs when the body either doesn’t produce enough insulin or can’t effectively use the insulin it produces. Insulin is a hormone that helps cells take in glucose from the blood to use for energy.

There are two main types:

  • Cause: It is an autoimmune condition where the body’s immune system attacks insulin-producing cells in the pancreas. As a result, the pancreas produces little to no insulin.
  • Insulin dependence: Type 1 diabetes is insulin-dependent. People with this condition need to take insulin injections or use an insulin pump because their body can’t produce insulin on its own.
  • Onset: It typically starts in childhood or young adulthood but can develop at any age.
  • Cause: In type 2 diabetes, the body either becomes resistant to insulin or doesn’t produce enough insulin to maintain normal blood sugar levels. It is more commonly associated with lifestyle factors such as obesity, poor diet, and lack of exercise.
  • Insulin dependence: It is considered non-insulin-dependent in its early stages, as it can often be managed with lifestyle changes and oral medications. However, over time, some people may require insulin therapy.
  • Onset: This form is more common in adults, particularly those over the age of 45, but it is increasingly being diagnosed in younger people due to rising obesity rates.
  • Type 1 diabetes: Always requires insulin, so it’s insulin-dependent.
  • Type 2 diabetes: Initially non-insulin-dependent but may progress to require insulin therapy.
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2
Q
  1. Differentiate diabetes mellitus and diabetes insipidus?
  2. Diabetes mellitus affects which organs?
    And can lead to
  3. What is meant by scarcity in plenty in diabtes mellitus?
  4. What kind of metabolic hormone is insulin?
  5. 1st hormone to be isolated and sequenced & to be produced by recombinant DNA?
A
  1. Diabetes mellitus is a disorder related to high blood sugar due to insulin problems, affecting metabolism. It includes type 1 (insulin-dependent) and type 2 (often non-insulin-dependent initially).

Diabetes insipidus is unrelated to blood sugar and involves excessive thirst and urination due to problems with the hormone ADH, affecting water balance, not glucose levels.

  1. Eye —- blindness
    Kidney—- renal failure
    Nervous system
    Can lead to;
    Heart attack
    Apmutation
  2. Despite hyperglycemia… Body cells are starved of glucose because no insulin to enter the glucose into cell
  3. Anabolic
    (Synthesis of glycogen, triacylglycerols & proteins)
  4. Insulin
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3
Q
  1. Molecular weight of insulin?
  2. Insulin contains how many amino acids?
  3. How many chains? With how many amino acids?
  4. Both chains are held by?
A
  1. 5,734
  2. 51
  3. 2 chains
    Chain A —- 21
    Chain B —- 30
  4. 2 Interchain disulphide bridges between
    A7 & B7
    A20 & B19
    1 interchain disulfide in chain A between
    Amino acid 6 & 11
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4
Q
  1. Gene for insulin synthesis is locate on ?
  2. Precursors for insulin synthesis?

3.molecular Weight of precursors?

  1. A useful index for endogenous production of insulin?
  2. Insulin forms complexes in B-cells by combining with?
A
  1. Chromosome 11
  2. Preproinsulin (110 amino acids)
    Proinsulin (86 amino acids)
    Active hormone insulin
    And connecting peptide
  3. Preproinsulin — 11,500
    Proinsulin — 9,000
  4. C-peptide
  5. Zinc
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5
Q
  1. Units of insulin secreted daily by pancreas?
  2. Normal insulin concentration in plasma?
  3. Most predominant factor for insulin release?
  4. Most potent amino acids for insulin release?
  5. Insulin is supressed/inhibited by?
    Stimulated by?
A
  1. 40-50
  2. 2-20 uU/ml1
  3. When glucose is administered orally
  4. Arginine
    Leucine
  5. Inhibition—Epinephrine
    Stimulataion—
    Glucose
    Aminoacids
    GI hormones
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6
Q
  1. In the plasma insulin has a normal half-life of?
  2. Enzyme that degrades insulin found in?
  3. Tissues that donot require insulin for glucose update (glucose can enter freely)?
  4. Which require insulin for gkucose uptake?
A
  1. 4-5 minutes
  2. insulinase — in liver & kidney
  3. Brain
    Kidney
    RBCs
    Retina
    Nerve
    Blood vessels
    Intestinal mucose
    Liver (not uptake but utilization is stimulated by insulin)
  4. Muscles
    Adipose tissue
    Leukocytes
    Mammary glands
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7
Q
  1. Insulin reduced ketogenesis by?
  2. How insulin effects lipolysis?
  3. How it effects lipogenesis?
  4. How insulin promotes cell growth and replication?
  5. The most sensitive tissue to insulin?
A
  1. Decreasing activity of HMG CoA synthetase
    Reduces release of fatty acids from stored fat and decrease ketone body production
  2. Decreases— to reduce free fatty acids —- by decreasing activity of hormone sensitive lipase
  3. Favours synthesis of TAG from glucose
    Provides more
    Glycerol 3 phosphate (from glycolysis)
    NADPH (from HMP shunt)
  4. Through
    Epidermal growth factor (EGF)
    Platelet Derived Growth Factor (PDGF)
  5. Adipose tissue
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8
Q
  1. How insulin starts its action?
    2.structure of insulin receptor?
    How many subunits? Molecular weight?
    Held together by?

3.Significance of subunits?

  1. Tyrosine kinase also activates?
  2. How insuline effects glucose ttansport?
  3. Insulin promotes synthesis of which enzymes?
A
  1. By binding with insulin receptors on plasma membrane
  2. Tetramer
    4 subunits of 2 types
    a2B2
    alpha (135,000)—extracellular
    Beta (95,000)—transmembrane
  3. Alpha— insulin binding site
    Beta — tyrosine kinase activity
  4. Insuline receptor substrate
  5. Intracellular Vesicles with GLUT transporter bind with plasma membrane
  6. Glucokinase
    Phosphofructokinase
    Pyruvate kinase
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9
Q
  1. Effect of epinephrine on insulin and glucagon?
  2. Glucagon is secreted by which cells?
  3. Glucagon structure?
    Amino acids
    Molecular weight
    Chains
  4. Glucagon is secreted has?
  5. Unlike insulin, the amino acid sequence of glucagon is?
  6. Effect of glucagon on liver??
  7. Action of glucagon is mediated thru?
  8. Action of glucagon on metabolism of;
    Lipid
    Proteins
A
  1. Insulin—- inhibits release
    Glucagon—-promoted release

Net effect: raises blood glucose level

  1. a-cells of pancreas
  2. 29 amino acids
    3,500
    A single chain
  3. Proglucagon (9,000 mw)
  4. Same in all the mammalian species
  5. Promotes;
    Gluconeogenesis
    Glycogenolysis
  6. Cyclic AMP
  7. Lipid —- promotes fatty acid oxidation —ketogenesis

Proteins — amino acid uptake by liver— gluconeogenesis

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10
Q
  1. Human body contains how much free glucose?
  2. Liver of an adult has how much stored glycogen?
  3. Liver is capable of producing how much glucose;
    Per minute
    Per 24 hours?

4.percent of Plasma glucose compared to blood glucose?

A
  1. 18g
  2. 100g
  3. 125-150 mg/min
    180-220 g/24 hrs
  4. Plasma glucose is slightly higher (15%) than blood glucose
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11
Q
  1. Fasting blood glucose level?
    Plasma glucose level?
  2. Following the ingestion of a carb meal, the blood glucose level may rise to?
  3. Fasting blood glucose level in
    Rumnants
    Birds
  4. Precursors for gluconeogenesis?
  5. Cori cycle?
A
  1. Blood—-70-100 mg/dl
    Plasma—-80-120 mg/dl
  2. 120-140 mg/dl
  3. Rumnants (lower)
    Sheep (30-40 mg/dl)
    Cattle (50-60 mg/dl)

Birds (higher)
(250-300 mg/dl)

  1. Lactate
    Free glycerol
    Propionate
    Some amino acids
  2. Conversion of muscle lactate to glucose in liver
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12
Q
  1. When glucose is predominantly derived from;
    Glycogenolysis
    Gluconeogenesis
  2. An adult liver can provide how much glucose from glycogen?
  3. What is TmG? Value?
  4. Renal threshold for glucose?
  5. At rest how much glucose is absorbed by
    Brain
    RBC and skeletal.muscles
A
  1. Glycogenolysis —- between the meals
    Gluconeogenesis — late night after depletion of hepatic glycogen
  2. 40-50 g
  3. The maximum ability of the renal tubules to reabsorb glucose/min is known as tubular maximum for glucose (TmG)
    Value —- 350 mg/min
  4. 160-180 mg/dl
    (If more than this value—glucose excreted in urine)

Brain —– 2/3rd
RBC and skeletal.muscles —– remaining 1/3rd

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13
Q
  1. Drug that cause secretion of insulin?
  2. Insulin is basically what type of hormone?
  3. What are incretins??
    Give examples?
  4. Net effect of hormones on blood glucose?
    Epinephrine
    Thyroxine
  5. Hormones produced by
    Adrenal cortex
    Adrenal medulla
  6. How glucocorticoids elevate blood glucose level?
A
  1. Tolbutamide
  2. Hypoglycemic (lowers blood glucose)
  3. Group of hormones that;
    Increase insulin release
    Decrease glucagon release

E.g;
Glucagon-like peptide (GLP-1)
Gastric inhibitory peptide (GIP)

  1. Epinephrine—- Increases
    Thyroxine—- Increases
  2. Adrenal cortex —- glucocorticoids
    Adrenal medulla —- epinephrine
  3. Protein metabolism —– gluconeogenesis —– inhibit glucose utilization by extrahepatic tissues
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14
Q
  1. Effect of Growth hormone and ACTH on glucose level??
  2. Net effect of insulin and other hormones? Which is stronger?
  3. Hypoglycemia occurs when blood glucose level?
  4. Types of hypoglycemia? Just name?
A
  1. Hyperglycemic
    GH—- dec. Uptake of glucose by certain tissues (muscles and adipose tissue)
    ACTH —- dec. Utilization of glucose
  2. Insulin— hypoglycermic
    All other — hyperglycemic
    Insulin is stronger
  3. Falls to less than 45 mg/dl

4.
• Post-prandial (reactive hypoglycemia)
• Fasting hypoglycemia
• Hypoglycemia due to alcohol intake
• Hypoglycemia due to insulin overdose
• Hypoglycemia in pregnancy and in neonates

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15
Q
  1. What is post prandial (reactive hypoglycemia)?
  2. How alcohol consumption can cause hypoglycemia?
  3. Hyoglycemia in premature and low-birth weight babies occurs due to?
  4. Whipple’s triad diagnosis of hypoglycemia?
  5. Significance of whipple’s triad?
A
  1. Elevated insulin secretion following a meal
  2. Effects the liver
    Reduces gluconeogenesis;
    NADH diverts gluconeogenesis substrates (puruvate, oxaloaxetate) to form
    Pyruvate —– lactate
    Oxaloacetate —- malate
  3. Lower liver stores of glycogen
    Less developed enzyme machinery of gluconeogenesis
  4. (SLR)
    Symptoms of hypoglycemia
    Low plasma glucose level at the time of symptoms
    Relief of sympyoms on administartion of glucose
  5. To separate true hypoglycemia from other conditions like idiopathic postprandial syndrome
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16
Q

1.which one is the juvenile diabetes and adult onset diabetes

  1. Give a characterization of NIDDM?
  2. How obesity can act as diabetogenic factor?
  3. what are the causes of insulin resistence? Give 2?
A
  1. Juvenile —– type 1 (IDDM)
    Adult onset —- type 2 (NIDDM)
  2. Mainly due to insulin resistence
    Reduction in GLUT 4 —– decreased response of target cell to insulin
  3. leads to decrease in insulin receptors on insulin responsive target cells
  4. Increased levels of;
    Tumor Necrosis alpha (TNF-a)
    Resistin
    Reduced secretion of;
    Adenopectin by adipocytes of obese people
17
Q
  1. A person is said to be suffering from diabetes if
    Fasting plasma glucose exceeds?
    And at 2hrs is?
  2. Normal plasma glucoze level range??
    After oral administration?
  3. Glucose clearance test (GTT) is done to ?
    Preferably done in the?
A
  1. Fasting plasma glucose exceeds —- 126 mg/dl
    And at 2hrs is — 200 mg/dl
  2. 75-110 mg/dl
    After oral— reaches peak value 140
    Returns to normal after 2 hrs
  3. Measure how well glucose ia processed by the body
    If efficient processing, glucoze level become high after oral administration but then quickly return to normal
    - in the morning
18
Q
  1. How latent diabetes is detected?
  2. How glucose is tested in individuals with glucose malabsorption?
  3. Commonest cause of glucosuria?
A
  1. By employing corticosteroid stressed GTT
  2. Intravenous GTT is carried out
  3. Diabetes mellitus
19
Q
  1. Differentiate renal glycosuria and alimentary glycosuria?
A
  1. Renal glycosuria and alimentary glycosuria are both conditions where glucose appears in the urine, but they occur for different reasons:
  • Cause: Happens due to a problem in the kidneys. The kidneys have a lower threshold for glucose, meaning they release glucose into the urine even when blood sugar levels are normal.
  • Blood Sugar Levels: Blood sugar levels are usually normal.
  • Reason: The kidneys fail to reabsorb glucose properly.
  • Common Issues: It’s often harmless and not related to diabetes.
  • Cause: Occurs after eating a large amount of sugar or carbohydrate-rich foods, leading to a temporary spike in blood sugar.
  • Blood Sugar Levels: Blood sugar levels become temporarily elevated after eating.
  • Reason: The body absorbs glucose quickly, overwhelming the normal ability to process it.
  • Common Issues: It’s usually temporary and linked to diet, not kidney function.

In short, renal glycosuria is a kidney-related issue, while alimentary glycosuria is due to eating lots of sugar or carbs, causing a temporary rise in blood sugar.

20
Q
  1. Why ketocidosis is assocaited with diabetes mellitus?
  2. Name metabolic changes with diabetes?
A
  1. As there is no insulin to use glucose for energy… Body makes ketone bodies leading to ketoacidosis
  2. •Hyperglycemia
    •Ketoacidosis
    •Hypertriglyceridemia (high VLDL, Chylomicrons)— hypercholesteremia
    • Glucose toxicity
    (Osmotic effects
    B-cell damage by free radicals
    Glycation of proteins)
21
Q
  1. Long term effects of diabetes?
  2. What are the 2 catergories of antidiabetic drugs?
  3. 2 types of commercially prepared insulin?
  4. Define glycation?
    Give example of most abundant glycated Hemogmobin?
A
  1. Diabetic neuropathy (peripheral nervous system)
    Diabetic nephropathy (renal failure)
    Diabetic retinopathy (transparent eye lens —- blindness)
  2. Sulfonylureas (TAG)
    (Secrete insulin)
    Tolbutamide
    Acetohexamide
    Glibenclamide

Biguanides (MP)
(Enhance insulin sensitivity)
Metformin
Phenoformin

  1. Short-acting — unmodified—last for 6 hours
    Long acting—- modified
    (Adsorption to protamine)
  2. Post translational, non-enzymatic addition of sugar residue to amino acids of proteins
    - most abundant - HbA1c
22
Q
  1. How HbA1 c is synthesized?
  2. Diagnostic importance of HbA1c?
  3. Normal HbA1c?
    Diabetic?
  4. How fructosamine can be measured in diabetics?
A
  1. By condensation of glucose with N-terminal valine of each B-chain of HbA
  2. Indication of blood glucose level over a period (reflects blood glucose level over 3 months prior to its measurement
  3. Normally—- 4-5.6%
    Diabetic —- 15%
  4. Glycated (glucose with albumin) serum protein measures glucose over a shorter period (2-3 weeks) compared to Hb (3 months)
    As albumin as shorter life-span as compared to RBC
23
Q
  1. Define microalbuminuria?
  2. Another alternative method for albumin estimation?
  3. Oral antidiabatic drugs used in diabetic patients include?
  4. In which type of diabetes mellitus, ketone bodies are common?
  5. What is insulinoma?
A
  1. Excretion of 30-300 mg of albumin in urine per day
    (Normally: 2.5-30)
    (Macroalbuminuria: > 300 mg/day
  2. Albumin creatinine ratio
    Normally: 30ug/mg creatinine
    Albuminuria: >300 ug/mg creatinine
  3. Glibenclamide
    Glimepiride
    Gliclazide
  4. Type 1
    Insulin dependent diabetes mellitus (IDDM)
  5. A rare tumors of B-cells of pancreas
    Leads to uregulated insulin secretion and hypoglycemia

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