An 8-month-old infant is brought in with poor feeding, lethargy, hypotonia, and hepatomegaly. Labs reveal hypoglycemia and metabolic acidosis. Which condition is most likely?

Hereditary fructose intolerance

Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency

Insulin dependent glucose uptake occurs in:

Epithelial cells of small intestine

Which of these is true about SGLT1?

Secondary active transport of glucose in intestine

Secondary active transport of glucose in prostate

Secondary active transport of glucose in brain

Secondary active transport of glucose in rods and cones

Glucose is primarily absorbed from which part of the small intestine?

Proximal part of the small intestine

Distal part of the small intestine

Glucose Transporters for NEET-PG: High-Yield Biochemistry Lessons

Glucose Transporters: Overview & Families - Sweet Gates

Membrane proteins vital for transporting glucose across cell membranes.
Essential as polar glucose cannot readily cross the hydrophobic lipid bilayer.
Two primary families:
- GLUT (GLUcose Transporter) family: Facilitated diffusion (passive transport).
- SGLT (Sodium-GLucose Transporter) family: Secondary active transport (co-transports glucose with $Na^+$).
Key players in maintaining systemic glucose homeostasis.

⭐ Glucose, being a polar molecule, cannot diffuse freely across the lipid bilayer and requires specific carrier proteins.

GLUT Family (Facilitated Diffusion) - The Facilitators

GLUT transporters (SLC2A gene family) mediate facilitated glucose diffusion. These integral membrane proteins exhibit tissue-specific expression and varying kinetic properties ($K_m$ values), crucial for glucose homeostasis.

Transporter	Gene	Key Locations	Approx. $K_m$ & Affinity	Specific Functions/Notes	Clinical/Mnemonic (📌)
GLUT1	SLC2A1	RBCs, brain, placenta	Low ($K_m \approx \textbf{1-2 mM}$), high affinity	Basal glucose uptake; Blood-Brain Barrier (BBB).	📌 "One for all" (basal). De Vivo disease.
GLUT2	SLC2A2	Liver, Pancreas ($\beta$-cells), kidney, gut (basolateral)	High ($K_m \approx \textbf{15-20 mM}$), low affinity	Glucose sensor (pancreas); high-capacity, bidirectional (liver).	📌 "Two-way street". Fanconi-Bickel syndrome.
GLUT3	SLC2A3	Neurons, placenta	Very Low ($K_m < \textbf{1 mM}$), very high affinity	Main neuronal glucose uptake.	📌 "Three for brain's glee".
GLUT4	SLC2A4	Skeletal muscle, adipose tissue, heart	Moderate ($K_m \approx \textbf{5 mM}$), medium affinity	Insulin-regulated glucose uptake.	📌 "Four for more" (insulin). Type 2 DM.
GLUT5	SLC2A5	Small intestine (apical), testes, kidney	Fructose specific ($K_m \approx \textbf{6 mM}$ for fructose)	Primarily fructose transporter.	📌 "Five for Fructose". Fructose malabsorption.
GLUT7	SLC2A7	Endoplasmic Reticulum (liver, gluconeogenic tissues)	Low $K_m$	Glucose export from ER (gluconeogenesis/glycogenolysis).	Key in hepatic glucose production.

SGLT Family (Secondary Active Transport) - The Co-Riders

Mechanism: $Na^+$-glucose cotransport (symport). Energy from electrochemical $Na^+$ gradient (via $Na^+$/$K^+$-ATPase).

Feature	SGLT1	SGLT2
Gene (SLC5A)	SLC5A1	SLC5A2
Location	Intestine (absorption), Kidney (PCT S3)	Kidney (PCT S1/S2)
Stoichiometry	2 $Na^+$ : 1 Glucose	1 $Na^+$ : 1 Glucose
Affinity/Capacity	↑ Affinity, ↓ Capacity	↓ Affinity, ↑ Capacity (bulk reabsorption)
Key Role	Glucose-galactose absorption; Final renal glucose capture	Reabsorbs ~90% filtered renal glucose
Clinical Note	Mutations: Glucose-galactose malabsorption	Target for SGLT2 inhibitors (e.g., -gliflozins)

⭐ SGLT2 inhibitors (e.g., canagliflozin, dapagliflozin, empagliflozin) are antidiabetic drugs promoting urinary glucose excretion by blocking glucose reabsorption in proximal renal tubules.

Clinical Significance & Regulation - Sweet Malfunctions & Masters

Regulation
- Insulin: ↑ GLUT4 translocation (muscle, adipose), ↑ glucose uptake.
Genetic Disorders
- GLUT1 Deficiency (De Vivo): Low CSF glucose, seizures, dev. delay. Ketogenic diet.
  
  ⭐ GLUT1 Deficiency Syndrome typically presents with infantile seizures, developmental delay, microcephaly, and is managed with a ketogenic diet to provide an alternative fuel source for the brain.
- Fanconi-Bickel (GLUT2): Impaired glucose/galactose use; hepatorenal glycogen, rickets, FTT.
- Glucose-Galactose Malabsorption (SGLT1): Neonatal osmotic diarrhea (glucose/galactose). Fructose diet.
  - 📌 SGLT1: Salty Gut Loses Two (Glucose, Galactose).
Pharmacology
- SGLT2 inhibitors (-gliflozins): Block renal glucose reabsorption (PCT); for T2DM, HF.
- Targeting GLUTs (e.g., GLUT1): Potential in cancer therapy.

High‑Yield Points - ⚡ Biggest Takeaways

GLUT1: Key for RBCs & brain; basal glucose uptake; insulin-independent.

GLUT2: Liver, pancreatic β-cells; high Km (low affinity), high capacity; glucose sensor.

GLUT3: Neurons, placenta; low Km (high affinity); ensures brain's glucose supply.

GLUT4: Skeletal muscle, adipose tissue; insulin-dependent; translocates to membrane with insulin.

GLUT5: Small intestine (jejunum); primarily a fructose transporter.

SGLT1: Small intestine, kidney; Na+-glucose cotransporter (active); absorbs glucose & galactose.

SGLT2: Kidney (PCT); Na+-glucose cotransporter; reabsorbs glucose; target for gliflozin drugs.

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