Omics era in type 2 diabetes: From childhood to adulthood

Table 1 Main findings of the omics studies in animal models

Ref.	Experimental design	Main findings
Eid et al[33]	Examination of changes in glucose and lipid metabolism in the kidney, eye and nerve of leptin receptor KO BKS db/db mouse model	Glycolytic genes were uniformly upregulated in kidney and peripheral nerves; glycolytic metabolites were increased in kidney and retina but decreased in the peripheral nerve. Kidney and nerves showed an overall trend towards increased levels of different lipid species, while in the retina lipid content was decreased
Chen et al[32]	Evaluation of the characteristic of lipid species in serum and tissues in a diabetic mouse model fed a high fat diet and treated with streptozocin by using LC/HRMS and MS/MS	Brain and heart showed the largest reduction in cardiolipin levels, while the kidney had more alteration in triacylglycerol levels. Cardiolipin with highly polyunsaturated fatty acyls decreased only in the atrium but not in the ventricle; similarly, renal cortex showed longer fatty acyl chains both for increased and decreased triacylglycerol species than renal medulla
Guitton et al[25]	Systematic review about the role S1P in the development of T2D and obesity	SphK1 KO in rat pancreatic β-cells and in INS-1 cells resulted in both lowered glucose-stimulated insulin secretion and insulin content associated with decreased insulin gene expression. Conversely, SphK1 overexpression restored both insulin synthesis and secretion. HFD-fed SphK1 ko mice also showed a reduction of β-cells size, number and mass due to lipotoxic condition

T2D: Type 2 diabetes; HFD: High fat diet; LC/HRMS: Liquid chromatography high-resolution tandem; MS: Mass spectrometry.