BD-AcAc2

Sprague Dawley (male, 7 weeks old, 180-200 g, chronic ulcerative colitis induced by 2% DSS for 7 days, followed by 1% DSS for 10 days, then 2% DSS for 7 days)^[1]

4% w/w

p.o.; ad libitum; 24 days

Increased plasma β-hydroxybutyrate levels, achieving nutritional ketosis.
Significantly reduced the percentage of body weight loss compared to DSS-only rats.
Significantly decreased the colon weight-to-length ratio compared to DSS-only rats.
Significantly reduced the disease activity index and macroscopic damage index compared to DSS-only rats.
Increased survival rate compared to DSS-only rats.
Significantly lowered the colonic inflammation score compared to DSS-only rats.
Significantly suppressed DSS-induced increases in ROS and MDA levels, and significantly reversed DSS-induced decreases in SOD and reduced GSH levels.
Significantly reduced DSS-induced increases in colon tissue levels of pro-inflammatory cytokines TNF-α, IL-6, IL-1β, and IL-18, and reduced IL-4 levels.
Significantly reversed DSS-induced increases in MPO activity, NF-κB DNA binding activity, caspase-1 activity, and active caspase-3 levels.
Significantly reduced DSS-induced increases in NLRP3 mRNA expression, NLRP3 protein levels, and gasdermin D N-terminal fragment (NGSDMD) levels.
Significantly increased BECN1 levels and decreased p62 levels compared to DSS-only rats, indicating enhanced autophagy.
Significantly increased colon tissue levels of tight junction proteins ZO-1, OCLN, and CLDN5 compared to DSS-only rats.
Significantly reversed DSS-induced changes in gut microbiome composition: reduced relative abundance of Fusobacterium spp., Clostridium spp., and increased relative abundance of Bifidobacterium spp. and Lactobacillus spp.

Sprague Dawley rats (male, 7 weeks old, 180-200 g)^[1]

4% w/w

p.o.; 24 days

Increased plasma β-hydroxybutyrate levels, achieving nutritional ketosis.
Showed normal colonic mucosal architecture with regular rounded mucus-secreting glands and intact goblet cells, matching untreated normal rats.

C57BL/6J mice (male, 72 weeks of age, naturally aged to 83 weeks)^[2]

25% of dietary kcals

dietary; ad libitum; 9 weeks

Showed no within-group change in body weight over time.
Prevented within-group increase in fat mass over time.
Increased expression of 6 skeletal muscle genes and decreased expression of 23 skeletal muscle genes.
Reduced fatty acyl chains in triacylglycerol in skeletal muscle.
Increased levels of 11 skeletal muscle proteins and decreased levels of 33 skeletal muscle proteins compared to controls.

C57BL/6 mice (male, 20 g)^[3]

2.5; 5.0; 10.0 g/kg

p.o.; single dose (20 minutes before hyperbaric oxygen exposure)

Prolonged CNS oxygen toxicity seizure latency in a dose-dependent manner.
Increased mean seizure latency.
Significantly reduced hyperbaric oxygen-induced increases in brain malondialdehyde content.
Substantially alleviated hyperbaric oxygen-induced lung damage including congestion, inflammatory cell infiltration, and structural distortion, with only mild pulmonary vasodilation observed in treated groups.
Showed no effect on lung malondialdehyde content, as hyperbaric oxygen exposure did not affect this parameter.

Wistar rats (male, 250 g)^[4]

4 g/kg

i.g.; single dose

Increased urethane-corrected PTZ seizure threshold.
Raised blood βHB levels.
Confirmed a significant treatment effect on PTZ threshold.

C57BL/6J mice (male, 5 weeks of age at study start, HFD-induced obesity)^[5]

30% of dietary energy

p.o.; 12 weeks

Reduced final body weight.
Reduced final fat mass.
Lowered mean energy intake.
Increased adjusted resting energy expenditure (REE) and total energy expenditure (TEE) significantly compared to pair-fed controls.
Increased adjusted dark cycle REE and TEE compared to both continuous HFD and pair-fed controls.
Elevated circulating β-hydroxybutyrate concentration to 0.51 mM, higher than continuous HFD and pair-fed controls.
Increased mRNA expression of uncoupling protein-1, deiodinase-2, and peroxisome proliferator-activated receptor γ coactivator-1α in interscapular brown adipose tissue (BAT) compared to pair-fed controls.
Increased UCP1 protein expression in BAT compared to pair-fed controls.
Reduced hepatic triglyceride levels.
Lowered fasting serum insulin.
Decreased glucose tolerance test incremental area under the curve (AUCI) and insulin tolerance test AUCI compared to continuous HFD controls, similar to pair-fed controls.