AMP-Activated Protein Kinase

Preclinical studies suggest activation of AMPK and PPAR-γ pathways, reported to enhance peripheral glucose uptake; clinical translation not yet established.

Investigated in preclinical models for GLP-1 pathway interaction and AMPK activation; clinical data lacking.

Studies report arctigenin as the most potent bioactive component of A. lappa; in vitro and preclinical data indicate modulation of NF-κB signalling, suppression of TNF-α and IL-6, and inhibition of COX-2/PGE2 pathways. AMPK activation has also been reported in preclinical models.

Root inulin content is associated with prebiotic properties and has been investigated in relation to metabolic pathways including AMPK and PPAR-γ activity in preclinical models.

In vitro evidence suggests AMPK activation and PPAR-γ agonism relevant to metabolic contexts; anti-inflammatory activity via NF-κB and COX pathways reported in preclinical models (Zhang et al. 2018)

Proposed as a contributor to cardiometabolic effects in preclinical data; clinical relevance in caper preparations not directly established (Annaz et al. 2022)

Potent α-glucosidase inhibitor; studies report inhibition of intestinal carbohydrate digestion, with downstream effects on postprandial glucose. Investigated for AMPK activation and insulin-sensitising mechanisms in preclinical models.

Investigated in preclinical models for effects on glucose metabolism and lipid regulation, reportedly via AMPK activation.

In vitro studies report induction of apoptosis in HL-60 leukemia cells and cytotoxic activity; proposed mechanisms include modulation of apoptotic signalling pathways.

Animal studies report hypoglycaemic and anti-hyperglycaemic activity attributed to multiple constituents; mechanistic pathways remain under preclinical investigation.

Activates AMPK (insulin-sensitizing, lipid-lowering), provides modest DPP-4 inhibition, modulates gut microbiota, and inhibits intestinal disaccharidases — collectively the basis for its glucose-lowering effect.

Direct AMPK activator — chemically and mechanistically the closest plant analog to metformin. Cochrane-level evidence in T2DM. Potent CYP3A4 / 2D6 / P-glycoprotein inhibitor — driver of the rich drug-interaction profile.

Studies report ABA activates lanthionine synthetase C-like 2 (LANCL2), with downstream AMPK activation proposed as a mechanism for observed improvements in postprandial glucose and insulin responses (Atkinson et al., 2019).

Studies report berberine activates AMPK, modulates PPAR-γ and insulin receptor signalling, and suppresses NF-κB-mediated inflammatory cascades; investigated in glycaemic regulation and metabolic contexts.

Preclinical data suggest ginsenosides may modulate insulin secretion via pancreatic KATP channel activity, enhance peripheral glucose uptake through AMPK activation, and sensitise the insulin receptor — proposed mechanistic basis for the postprandial glycemia effects reported in clinical trials.

Olas et al. (2024) and Prasertsri et al. (2025) report that ecdysteroids such as 20-hydroxyecdysone found in A. officinalis root extract exhibit antioxidant and anti-inflammatory activities; in vitro and animal data suggest modulation of NF-κB signalling and AMPK-related metabolic pathways, though human mechanistic confirmation is limited.

Preclinical reports describe inhibition of COX-2 and 5-LOX, suppression of NF-κB, and AMPK activation relevant to metabolic signalling (Zhao et al., 2019; Wang et al., 2018).

Primary bioactive compound in Nigella sativa essential oil. Multi-target — AMPK activation parallels metformin/berberine; NF-κB inhibition is broad anti-inflammatory.

Improves insulin receptor sensitivity, activates AMPK, and inhibits GSK-3β — collectively enhancing GLUT4-mediated glucose uptake. Also has direct antimicrobial activity.

Preclinical literature cited in He et al. 2014 associates chlorogenic acid with anti-inflammatory and antioxidant activity, including NF-κB modulation.

Preclinical data suggest anthocyanins may modulate insulin receptor signalling and AMPK activation; anti-inflammatory activity via NF-κB inhibition has been reported in vitro (Chhikara et al., 2018).

Reviews describe inhibition of COX-2 and NF-κB and activation of AMPK in vitro; clinical relevance at consumed doses is unestablished.

In vitro and animal studies report that the PMI-5011 ethanolic extract and its constituent DMC-2 may improve insulin sensitivity via AMPK activation and PPAR-γ modulation; mechanisms were investigated in C57BL/6 mouse models and corroborated in a small human RCT.

Preclinical studies report modulation of glucose metabolism pathways and renoprotective activity in diabetic nephropathy models; mechanistic links to insulin signalling and AMPK activation are proposed in the literature.

Same compound as in standalone Berberine entries — direct AMPK activation. Goldenseal contains 0.5–6% berberine by dry weight.

Hypoglycemic via AMPK activation and improved insulin sensitivity; anti-inflammatory through NF-κB modulation. Mechanism overlaps with several other iridoid-rich herbs; basis for traditional use in 'yin deficiency' patterns including diabetes.

Preclinical data suggest scavenging of reactive oxygen species and possible xanthine oxidase inhibition; AMPK activation reported in cell models. Clinical translation not yet established.

Studies report berberine activates AMPK (sharing mechanistic overlap with metformin), may modulate insulin receptor signaling, and has been reported to suppress NF-κB-mediated inflammatory and pro-proliferative pathways in preclinical models. Effects on the GH/IGF-1 somatotropic axis reported in a veterinary study.

Antioxidant and putative anti-aging activity; basis for the herb's traditional use as a longevity tonic. Mechanism involves modest AMPK activation and SIRT1 modulation in preclinical models.

Insulin-sensitizing cyclitol; improves glucose handling in animal and in vitro models.

Mangiferin, a xanthone present in Swertia chirata, has documented compound-specific activation of AMPK (well-characterized in metabolic/antidiabetic studies). This is a named-compound, target-specific link rather than generic attribution.

Insulin-sensitizing via AMPK activation — galegine is the natural-product lead from which the biguanide drug class (metformin, phenformin, buformin) was developed in the 1920s. Galegine itself is too toxic for clinical use, but the discovery launched modern type-2-diabetes pharmacology.