Computational pharmacokinetics and in vitro-in vivo correlation of anti-diabetic synergistic phyto-composite blend

Table 1 Possible therapeutic molecular targets for type 2 anti-diabetic therapy

Type	Target for action	Nature of action	Effect produced
Protein kinases	Protein kinase C	Inhibitory	Block receptor desensitization
	AMP activated kinase	Activator	Enhance glucose transport
	GSK-3	Inhibitory	Activate glycogen synthase
	MAP kinase	Inhibitory	Block receptor desensitization
Protein phosphatases	PTP-1b	Inhibitory	Block receptor dephosphorylation
	PP1	Activator	Activate glycogen synthase
	LAR	Inhibitory	Block receptor dephosphorylation
Lipid phosphatases	PTEN	Inhibitor	Increase PIP3-stimulated glucose transport
Cell surface receptors	Insulin receptor	Agonist	Insulin mimetic
	Glucagon receptor	Antagonist	Low fasting glucose
	GLP receptor	Agonist	Increase insulin secretion
	β-3 adrenergic receptor	Agonist	Increase lipolysis
Ion channels	Sulphonyl urea receptor	Inhibit K channel	Increase insulin secretion
Transcription factors	PPAR-γ	Selective modulator	Insulin sensitizer
	HNF4	Selective modulator	Increase insulin secretion

AMP: Adenosine monophosphate activated kinase; GSK-3: Glycogen synthase kinase 3; MAP: Mitogen activated protein; PTP-1b: Protein tyrosine phosphatase-1b; PP1: Protein phosphatase 1; LAR: Leukocyte antigen related; PTEN: Phosphatase and tensin homolog; PPAR-γ: Peroxisome proliferator-activated receptor; GLP: Glucagon-like peptide.