Table 2.
Beneficial effects of A. muciniphila and its derivatives supplementation on metabolic diseases.
| Viability of A. muciniphila |
Disease | Study grouping | Daily dose and period of administration | A. muciniphila validity conclusions | Ref. |
|---|---|---|---|---|---|
| A. muciniphila | HFD-fed obese mice | N = 6, HFD N = 6, HFD + AKK |
① HFD group: PBS ② HFD + AKK group:4.0× 108 CFU AKK ③ 6 weeks of oral administration |
↑glucose tolerance ↓adipose tissue inflammation |
(69) |
|
A.muciniphila, Heat-killed A. muciniphila |
High-fat, high- sucrose (HF/HS) diet induced obese mice |
N = 5, HF/HS + AKK N = 5, HF/HS + H-K-AKK |
① HF/HS+AKK group: 1.44 × 109 CFU/0.2 ml AKK; ② HF/HS+ H-K-AKK group: 1.44 × 109 CFU/0.2 ml H-K-AKK; ③ 5 weeks of oral administration. |
↓body weight; ↓total body fat; ↑metabolic parameters. |
(70) |
| A. muciniphila | HFD-fed obese mice | N = 4-5, HFD N = 4-5, HFD + AKK mucin (+) N = 4-5, HFD + AKK mucin (-) |
① HFD group: 0.15 ml sterile anaerobic PBS (containing 25% vol/vol glycerol); ② HFD +AKK mucin (+) group: 1 × 108 CFU/day (AKK grown on mucus-based medium); ③ HFD +AKK mucin (-) group: 1 × 108 CFU/day (AKK grown on mucus-depleted medium); ④ 4 weeks of oral administration. |
HFD +AKK mucin (-) group was more efficiently than HFD +AKK mucin (+) group in aspect of: ↓obesity; ↑barrier integrity. |
(71) |
| AmEVs | HFD induced a diabetic phenotype |
N = 5–7, ND N = 5–7, NCD + AmEVs N =5–7, HFD N = 5–7, HFD + AmEVs |
① ND and HFD group: PBS; ② NCD + AmEVs and HFD + AmEVs group: 10 μg per mice AmEVs ③ 2 weeks of oral administration. |
AmEVs: ↑: glucose tolerance; ↑: body weight; ↑: intestinal barrier function. |
(72) |
|
A.muciniphila; Pasteurized A.muciniphila |
HFD induced a diabetic phenotype |
N=11, placebo N=12, pasteurized AKK N=9, AKK |
① placebo group: placebo; ② pasteurized AKK group: 1*1010 CFU/day/volunteer; ③ 3 months of oral administration. |
↓: relevant blood markers of liver dysfunction and inflammation. | (73) |
|
A.muciniphila; Heat killed A. muciniphila |
Atherosclerosis | N=8-10, NCD N=8-10, Western diet (WD) N=8-10, WD + AKK N=8-10, WD + heat- killed AKK |
① NCD and WD group: 200 µl PBS; ② WD+ AKK and WD+ heat killed AKK group: 5×109 CFU/200 µl; ③ 8 weeks of oral administration. |
AKK reversed Western diet–induced exacerbation of atherosclerotic lesion formation without affecting hypercholesterolemia. |
(74) |
| A.muciniphila | Fatty Liver Disease | N=5, ND + PBS N=5, ND + AKK N=5, HFD + PBS N=5, HFD + AKK |
① ND+PBS and HFD+ PBS group: PBS; ② ND+ AKK and HFD+ AKK group: 108 to 109 CFU/ml; ③ 10 weeks of oral administration. |
↓: lowered serum triglyceride and alanine aminotransferase levels in obese mice; ↓: the expression of SREBP (regulator of TG synthesis in liver tissue). |
(75) |
| A.muciniphila | NASH | N=5-8, High-fat and high-cholesterol (HFC) N=5-8, HFC + AKK |
① HFC group: HFC diet+ 200 µl PBS; ② HFC + AKK group: HFC diet + 1 × 108 CFU/ml/200 µl, ③ 6 weeks of oral administration. |
↓: Hepatic steatosis/inflammatory ↓: serum ALT/AST/ALP ↓: hepatic genes expression related to steatosis and inflammation |
(76) |
| A.muciniphila | NASH-induced cognitive damage |
N=8, NC group N=8, HFHC + PBS N=8, HFHC + Lacticaseibacillus rhamnosus GG(LGG) N=8, HFHC + AKK |
① ND group: normal chow; ②HFHC + PBS group: HFHC +100 µl PBS; ③HFHC + LGG group: HFHC + 1*109 CFU/100 μl LGG; ④HFHC + AKK group: HFHC + 1*109 CFU/100 μl AKK; ⑤4 weeks of oral administration. |
↓: HFHC-induced cognitive dysfunction (including impaired spatial working memory and novel object recognition) |
(77) |
"↑" means promotion or enhancement; "↓" means reduction or alleviation.