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Molecular Docking Studies of Guggultetrol from Nymphaea pubescens with Glucokinase (GK)

Introduction

TypeII diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by hyperglycemia resulting from insulin resistance and impaired pancreatic cell function. Glucokinase (GK; EC2.7.1.2), a hexokinase isoform expressed in liver and pancreatic cells, acts as a glucose sensor and catalyzes the first step of glycolysis. Enhancing GK activity is a validated therapeutic strategy for lowering blood glucose levels.

Natural products continue to provide lead compounds for antidiabetic drug discovery. *Nymphaea pubescens* (the pink water lily) is traditionally used in Ayurvedic medicine for its antidiabetic properties. Phytochemical investigations have identified a unique flavonoidtype compound, guggultetrol, which exhibits promising hypoglycaemic activity in animal models. This page summarises a computational docking study that evaluates the binding affinity and interaction pattern of guggultetrol with human glucokinase.

Guggultetrol

Guggultetrol (C22H28O10) is a polyphenolic glycoside comprising a flavonoid core conjugated to a tetrahydroxyalkyl side chain. Its chemical structure is shown in Figure1.

Guggultetrol chemical structure
Figure1. Chemical structure of guggultetrol.

Key physicochemical properties (calculated):

PropertyValue
Molecular weight452.44Da
LogP (XlogP3)2.1
Hbond donors8
Hbond acceptors12
Rotatable bonds9

The high number of hydrogenbond donors/acceptors suggests strong capability for polar interactions with enzyme active sites.

Glucokinase (GK)

Human glucokinase (UniProt ID: P35557) is a monomeric enzyme of 465 residues. The active site is located in a deep cleft formed by the large and small domains. Critical residues for glucose binding include Asp205, Arg63, and Lys169, while allosteric sites (e.g., near the Cterminal tail) accommodate activators such as GKAs (glucokinase activators).

For docking, the crystal structure with PDB ID 1V4S (resolution 2.3) was selected because it contains an open conformation suitable for ligand accommodation.

Methodology

Protein preparation

  1. Downloaded PDB 1V4S from the Protein Data Bank.
  2. Removed heteroatoms, water molecules, and the cocrystallised ligand.
  3. Added missing hydrogen atoms and assigned the AMBER99SBILDN force field.
  4. Energyminimized the structure (10000 steps, steepest descent) using GROMACS 2023.

Ligand preparation

  1. Generated the 3D structure of guggultetrol with Avogadro and performed a geometry optimisation (MMFF94, 500 steps).
  2. Calculated Gasteiger charges and saved the ligand in MOL2 format.

Docking protocol

  • Software: AutoDock Vina 1.2.3.
  • Search space: centre (x=12.5, y=3.8, z=1.2) ; size=222222, encompassing the glucosebinding cleft and the allosteric pocket.
  • Exhaustiveness set to 24; pose clustering at 2.0 RMSD.
  • Docking repeated three times to ensure reproducibility.

Postdocking analysis

Binding affinities were ranked by Vina scores. The topranked pose was visualised with PyMOL and interaction fingerprints were generated using LigPlot+. Hydrogen bonds, stacking, and hydrophobic contacts were catalogued.

Results

Binding affinity

The best docking score for guggultetrol was 9.2kcalmol, comparable to the reference GK activator cyclohexylphenylpyrimidine (9.5kcalmol) and significantly better than glucose (5.8kcalmol).

Interaction profile

Interaction typeResidue(s)Distance ()
Hbond (donor)Asp2052.8
Hbond (acceptor)Arg632.9
Hbond (donor)Lys1693.0
stackingPhe1133.7
HydrophobicVal452, Ile211~4.0

Figure2 illustrates the docking pose. The flavonoid core occupies the glucosebinding pocket, forming a network of hydrogen bonds with Asp205, Arg63 and Lys169. The tetrahydroxy side chain extends toward the allosteric pocket, establishing additional contacts with His179 and the backbone carbonyl of Gly229. This dualsite occupation may explain the high binding affinity.

Docking pose of guggultetrol in GK
Figure2. Predicted binding mode of guggultetrol within glucokinase.

Discussion

The docking results suggest that guggultetrol can bind glucokinase with an affinity comparable to known synthetic activators. The extensive hydrogenbond network compensates for the moderate lipophilicity (logP2) of the molecule, while aromatic stacking with Phe113 stabilises the ligand orientation.

Importantly, the ligand bridges the catalytic and allosteric regions, a feature typical of bifunctional GK activators that show both increased Vmax and reduced Km for glucose. This structural insight aligns with invivo reports that *N. pubescens* extracts lower fasting blood glucose in diabetic rats.

Potential limitations:

  • Docking scores are approximations; molecular dynamics (MD) simulations would be required to assess stability over time.
  • The glycosidic moiety could be hydrolysed in vivo, altering activity.
  • Selectivity for GK versus other hexokinases was not evaluated.

Future work should include (i) 100ns MD simulations of the complex, (ii) freeenergy calculations (MMPBSA), and (iii) biochemical assays to confirm activation of GK by purified guggultetrol.

Conclusion

Computational docking indicates that guggultetrol, a flavonoid glycoside from *Nymphaea pubescens*, is a promising glucokinase binder with a predicted binding energy of 9.2kcalmol. The interaction pattern, involving key catalytic residues and an additional allosteric contact, supports its potential as a natural GK activator. These findings provide a rational basis for further experimental validation and may contribute to the development of plantderived therapeutics for typeII diabetes.

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