Schisandra Berry for Blood Sugar & Cholesterol?

Key Findings

This 2018 study demonstrated that Schisandra chinensis (Turcz.) Baill.-supplemented rice cookies (SRCD) significantly improved lipid and glucose metabolism in mouse models compared to regular rice cookies (RCD). In high-fat diet (HFD)-fed ICR mice, SRCD reduced plasma and hepatic triglyceride and cholesterol levels, downregulated genes involved in lipid synthesis (e.g., fatty acid synthase, HMG-CoA reductase), and upregulated genes related to beta-oxidation (e.g., PPARα) and cholesterol export (e.g., ABCG5/ABCG8). In db/db mice (a model of type 2 diabetes), SRCD enhanced glucose tolerance, regulated gluconeogenic enzymes (e.g., PEPCK, G6Pase), and modulated insulin signaling pathway biomarkers (e.g., increased IRS-1 and GLUT4 expression). Additionally, SRCD elevated antioxidant enzymes (e.g., SOD, CAT) and reduced inflammatory cytokines (e.g., TNF-α, IL-6), leading to lower oxidative stress, leptin, and insulin levels versus RCD or HFD alone (P < 0.05 for all outcomes).

Study Design

The study employed two animal models: ICR mice (for hypolipidemic effects) and db/db mice (for antidiabetic effects). ICR mice (n = 7/group) were fed one of four diets for 9 weeks: AIN-76 (control), HFD, RCD-supplemented HFD, or SRCD-supplemented HFD (10% w/w). db/db mice (n = 7/group) received HFD, RCD, or SRCD for 10 weeks. Plasma, hepatic, and molecular markers were analyzed post-intervention. The study was controlled and randomized but lacked details on blinding or sex/age demographics.

Dosage & Administration

Schisandra berry was incorporated into rice cookies at 10% weight/weight (w/w) concentration. Both RCD and SRCD were administered orally via the diet (mixed into HFD) at a dose equivalent to 10% of total dietary intake. The exact dosage per mouse (e.g., mg/kg body weight) was not reported.

Results & Efficacy

In ICR mice:
- SRCD reduced plasma triglycerides by 25% and total cholesterol by 30% compared to RCD (P < 0.05).
- Hepatic lipid synthesis genes were downregulated (e.g., SREBP-1c, FAS), while beta-oxidation genes (e.g., PPARα, CPT1) and cholesterol export genes (ABCG5/ABCG8) were upregulated (P < 0.05).

In db/db mice:
- Fasting blood glucose decreased by 18% in SRCD vs. HFD (P < 0.05).
- Glucose tolerance improved, with reduced AUC in oral glucose tolerance tests (P < 0.05).
- Insulin signaling pathway markers (IRS-1, PI3K, GLUT4) were upregulated, while gluconeogenic enzymes (PEPCK, G6Pase) were downregulated.
- Oxidative stress (MDA levels) decreased by 40%, and inflammatory cytokines (TNF-α, IL-6) were reduced by 35–50% in SRCD groups (P < 0.05).

Limitations

1. Small sample size: n = 7 per group may limit statistical power.
2. Animal model constraints: Results may not generalize to humans due to physiological differences.
3. Lack of dose-response data: Only one SRCD concentration (10%) was tested.
4. Unspecified active compounds: The study did not quantify lignans (e.g., schisandrin) in SRCD, limiting mechanistic insights.
5. Short duration: 9–10 weeks may not capture long-term efficacy or safety.
6. No baseline comparisons: SRCD’s effects were not compared to a non-HFD control in db/db mice.

Clinical Relevance

This study suggests Schisandra berry supplementation may synergistically enhance the metabolic benefits of rice cookies in managing dyslipidemia and diabetes. However, these findings are limited to mice and cannot be directly extrapolated to humans. For supplement users, the results highlight Schisandra’s potential to modulate lipid synthesis, inflammation, and glucose metabolism, but clinical trials are needed to validate these effects. The study supports further investigation into Schisandra-based functional foods, though practical applications remain speculative until human data are available.