|
Disease | Population studied | Samples | Platform | Biological processes associated with the metabolic disorder | Reference |
|
Obesity | Adolescents: (i) Normal weight () (ii) Obese () (iii) T2D () | Plasma | MS/MS | No defects in fatty acid and amino acid metabolism | Mihalik et al. [23] |
| Children: (i) Normal weight () (ii) Obese () (iii) Overweight () | Plasma | GC-MS | Changes in lipid metabolism |
Zeng et al. [24] |
Children: (i) Normal weight () (ii) Obese () | Serum | MS | Oxidative stress, changes in sphingomyelin metabolism, in -oxidation, and in pathways associated with energy expenditure. | Wahl et al. [25] |
| Obese children: (i) With substantial overweight reduction () (ii) Without substantial overweight reduction () | Serum | MS | Phosphatidylcholine metabolism | Wahl et al. [26] |
| Pigs (4 months of age): (i) Obese type () (ii) Lean type () | Serum | NMR | Lipogenesis, lipid oxidation, energy utilization and partition, protein and amino acid metabolism, and fermentation of gastrointestinal microbes | He et al. [27] |
|
Diabetes 1 | Children: (i) T1D () (ii) Control () | Urine |
1H-NMR | Increased glomerular filtration rateand/or a modification of the transport mechanisms at thetubular level. | Zuppi et al. [29] |
| Children: (i) Who progressed to T1D () (ii) Who remained healthy and autoantibody negative () | Serum | UPLC-MS | Dysregulation of lipid and amino acid metabolism preceding islet autoimmunity |
Orei et al. [30] |
| Children: (i) T1D () (ii) Control () | Urine | CE-UV | — | Balderas et al. [31] |
| Children: (i) T1D () (ii) Control () | Plasma Urine | LC-MS CE-MS | Dysregulation of lipid metabolism and activity of the gut microflora Protein and amino acid metabolism, glycation | Balderas et al. [32] |
| Children: (i) T1D () (ii) Control () | Urine |
1H-NMR | Carbohydrate metabolism and gut microbial metabolism | Culeddu et al. [33] |
(i) Diabetic children and teenagers with T1D () (ii) Control () | Urine |
1H-NMR | Endogenous glucose production pathway from proteins | Deja et al. [34] |
|
Inflammatory bowel disease | Mice (4–24 weeks of age) | Hydrophilic and lipophilic extracts from intestinal compartments | NMR LC-MS | Modifications of the general cell membrane composition, alteration of energy homeostasis, and the generation of inflammatory lipid mediators | Baur et al. [35] |
|
Celiac disease | Infants genetically susceptible for CD () | Stool | NMR | GI tract microbiota metabolism | Sellitto et al. [36] |
|