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Normal FBS and metabolic pathway

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Normal FBS and Glucose Metabolic Pathways

1. Normal Fasting Blood Sugar (FBS) Values

CategoryFasting Plasma Glucose
Normal70 - 99 mg/dL (4.1 - 5.5 mmol/L)
Impaired fasting glucose (Pre-diabetes)100 - 125 mg/dL
Diabetes mellitus≥ 126 mg/dL (on two occasions)
Hypoglycemia< 50 mg/dL (symptomatic threshold)
  • Fasting is defined as no caloric intake for at least 8 hours.
  • The Tietz reference interval for plasma/serum fasting glucose in adults is 74-99 mg/dL (4.1-5.5 mmol/L).
Sources: Lippincott's Biochemistry 8e; Textbook of Family Medicine 9e; Tietz Textbook of Laboratory Medicine 7e

2. Glucose Metabolic Pathways

Glucose 6-phosphate (Glucose 6-P) is the central branch point of carbohydrate metabolism. After phosphorylation by hexokinase (or glucokinase in liver/pancreatic beta cells), it can enter four major routes:
Glucose 6-P as a branch point - showing entry into glycolysis, pentose phosphate pathway, glycogen synthesis

A. Glycolysis (Aerobic / Anaerobic)

The primary ATP-generating pathway. Occurs in the cytoplasm of all cells.
Glycolysis two phases - preparative and ATP-generating
Two phases:
Phase I - Preparative Phase (energy investment)
  1. Glucose + ATP → Glucose 6-P (by hexokinase/glucokinase) - commits glucose to the cell
  2. Glucose 6-P → Fructose 6-P (phosphoglucose isomerase)
  3. Fructose 6-P + ATP → Fructose 1,6-bisphosphate (phosphofructokinase-1, the key regulatory step)
  4. Fructose 1,6-bisphosphate → 2x Glyceraldehyde 3-phosphate (aldolase)
  • Net investment: 2 ATP consumed
Phase II - ATP-Generating Phase 5. G3P + NAD⁺ + Pi → 1,3-bisphosphoglycerate + NADH (G3P dehydrogenase) 6. Substrate-level phosphorylation steps → 2x ATP per triose (x2 for two trioses) 7. Final product: 2 pyruvate
  • Net yield: 2 ATP + 2 NADH per glucose
Pyruvate fate (two routes):
  • Aerobic: Pyruvate → Acetyl-CoA (via pyruvate dehydrogenase) → TCA cycle → oxidative phosphorylation → ~30-32 ATP total
  • Anaerobic: Pyruvate → Lactate (allows NADH reoxidation to NAD⁺, sustaining glycolysis without oxygen)

B. Glycogen Metabolism

ProcessTriggerLocation
Glycogenesis (glycogen synthesis)Fed state, insulinLiver, muscle
Glycogenolysis (glycogen breakdown)Fasting, glucagon, epinephrineLiver (→ blood glucose), muscle (→ glycolysis)
  • In the postprandial state: liver stores excess glucose as glycogen via glycogenesis, then converts surplus to fat (lipogenesis)
  • In the fasting state: liver breaks down glycogen (glycogenolysis) to release glucose into the blood

C. Gluconeogenesis

Synthesis of new glucose from non-carbohydrate precursors - occurs mainly in the liver (and kidney).
Precursors: Amino acids (especially alanine), lactate, glycerol (from triglyceride breakdown)
Triggered by: fasting, glucagon, cortisol. This pathway is critical when blood glucose falls below normal.

D. Pentose Phosphate Pathway (HMP Shunt)

  • Generates NADPH (for reductive biosynthesis and glutathione reduction) and ribose 5-phosphate (for nucleotide synthesis)
  • Runs continuously in RBCs, liver, adrenal cortex, and lactating mammary gland
  • Important for protecting RBCs from oxidative damage (G6PD deficiency impairs this)

3. Hormonal Regulation of Blood Glucose

HormoneStateEffect
InsulinFedStimulates glycolysis, glycogenesis, lipogenesis; suppresses gluconeogenesis
GlucagonFastingStimulates glycogenolysis and gluconeogenesis in liver
EpinephrineStressInhibits glycogenesis; promotes glycogenolysis
CortisolProlonged fastPromotes gluconeogenesis; raises blood glucose

4. Role of the Liver in Glucose Homeostasis

The liver acts as the body's glucose buffer (Guyton & Hall). Key functions:
  1. Glycogen storage - absorbs excess post-meal glucose
  2. Gluconeogenesis - synthesizes glucose from amino acids and glycerol when blood glucose falls
  3. Conversion of galactose and fructose to glucose
  4. Formation of metabolic intermediates (pyruvate, acetyl-CoA) for other biosynthetic reactions
"Storage of glycogen allows the liver to remove excess glucose from the blood, store it, and then return it to the blood when the blood glucose concentration begins to fall too low" - Guyton and Hall Textbook of Medical Physiology
Sources: Guyton & Hall Textbook of Medical Physiology; Basic Medical Biochemistry 6e (Lieberman & Peet); Lippincott's Biochemistry 8e; Tietz Textbook of Laboratory Medicine 7e; Miller's Anesthesia 10e
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