Table 2.
Principal classes of brown seaweed compounds and metabolites with their relative biological effects in the context of MS comorbidities.
| Algal Component | Bioactive Compounds | Main Molecular Pathways | Refs. |
|---|---|---|---|
| Polyphenols | |||
| Phlorotannins | 2,5-dihydroxybenzoic acid, Phloroglucinol, Ishophloroglucin A | Inhibition of α-glucosidase, α-amylase and lipase, 3-hydroxy-3-methylglutaryl-CoA (HMGCoA) reductase. | [37,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56] |
| Fuhalols and Phlorethols: Octaphlorethol A, Triphlorethol-A | Downregulation of adipogenic specific proteins: PPARγ, SREBPs, C/EBPα, and adiponectin. | ||
| Fucols | Activation of Akt and AMPKα signaling. | ||
| Fucophlorethols: Phlorofucofuroeckol A | Downregulation of perilipin, TNFα, FABP4, FASN, FATP1, Leptin, and acyl-CoA synthetase 1. | ||
| Eckols and carmalols: Dieckol, 6,6′-Bieckol, 8,8′-Bieckol, 2-O-(2,4,6-trihydroxyphenyl)-6,6′-bieckol, Phloroglucinol-6,6-Bieckol, 2,7″-Phloroglucinol-6,6′-bieckol, Pyrogallol- Diphlorethohydroxycarmalol Eckol, Dioxindehydroeckol7-phloroeckol | ACE inhibition. | ||
| Up-regulation of GLUT4. | |||
| Downregulation of phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphatase (G6Pase), and gluconeogenesis-related enzymes. | |||
| Increase glycerol secretion. | |||
| Increase eNOS phosphorylation. | |||
| Bromophenols | 3,4-dibromo-5-(methoxymethyl)-1,2-benzenediol, | Inhibition of PTP1B activity. | [57,58] |
| 2-methyl-3-(2,3-dibromo-4,5-dihydroxy)-propylaldehyde | |||
| 3-(2,3-dibromo-4,5-dihydroxy-phenyl)-4-bromo-5,6-dihydroxy-1,3-dihydroiso-benzofuran | |||
| Polysaccharides | |||
| Alginates | Inhibition of α-amylase, pancreatic lipase and pepsin. | [42,59,60] | |
| Sulphated fucans | Inhibition of α-amylase and ACE, protective effects against ROS. | [61] | |
| Fucoidans | Inhibition of α-glucosidase and α-amylase. | [62,63,64,65] | |
| Inhibition of ACE. | |||
| Downregulation of hemoglobin A1c (HbA1c) levels. | |||
| Increase NO production, eNOS activation, and Akt phosphorylation. | |||
| Activation of PI3K/Akt/eNOS-dependent pathways. | |||
| Inhibition of adipocyte differentiation and basal lipolysis. | |||
| Acceleration of the mitochondrial β-oxidation, peroxisomal oxidation or degradation. | |||
| Modulation of RCT-related protein expression. | |||
| Upregulation of superoxide dismutase and catalase. | |||
| Laminarins | Upregulation of STAT1, STAT3, c-Jun, c-Fos, and COX-2 in macrophages. | [66,67,68,69,70] | |
| Lipids and Fatty acids | n-3 fatty acids | Inhibition of α-glucosidase and α-amylase. | [71] |
| Up-regulation of GLUT1 and GLUT4. | |||
| Increase insulin sensitivity. | |||
| Terpenoids | |||
| Carotenoids | Fucoxanthin | Decrease in lipid accumulation. | [38,72,73,74,75,76] |
| Inhibition of advanced glycation end product formation. | |||
| Inhibition of PTP1B activity. | |||
| Increase AGE formation. | |||
| Upregulation of PPARα, p-ACC, and CPT-1; modulation of IRS-1/PI3K/AKT and AMPK signaling. | |||
| Downregulation of adipogenic and lipogenic factors, such as CCAAT/C/EBPα, PPARγ, fatty acid-binding protein 4, diglyceride acyltransferase 1, and lysophosphatidic acid acyltransferase-θ. | |||
| UCP-1 upregulation in white adipose tissue. | |||
| Sterols | Fucosterol, Thunberol | Inhibition of PTP1B, human recombinant aldose reductase (HRAR), and α-glucosidase activity. | [46,77,78,79,80,81] |
| Downregulation of PPARγ and C/EBPα expression. | |||
| Inhibition of advanced glycation end product formation. | |||
| Peptides | Inhibition of α-glucosidase and α-amylase. | [82] | |
| Akt upregulation and PI3K/AKT phosphorylation. | |||
| ACE inhibition. | |||
| Alkaloids | Indole-2-carboxaldehyde | Downregulation of the SREBP-1c, PPARγ C/EBPα; inhibition of adipogenesis through AMPK activation. | [83] |
| Indole-6-carboxaldehyde | Inhibition of adipocyte differentiation and lipid accumulation. |