Educational supplement editorial for trendytones.org. This article summarizes published research and is not medical advice. Mulberry leaf extract and DNJ-standardized products are not FDA-approved to treat, cure, or prevent diabetes or any other disease. Talk with a qualified clinician before starting any supplement, especially if you use diabetes medications or have kidney or liver disease.
Introduction
Mulberry leaf—most often from *white mulberry (Morus alba L.)—has a long history in East Asian food and traditional medicine. In modern dietary supplements, interest centers on mulberry leaf extract (MLE), frequently standardized to the iminosugar 1-deoxynojirimycin (DNJ). DNJ is a glucose analogue that can inhibit intestinal α-glucosidase* enzymes, slowing digestion of dietary starch and sucrose and blunting the rise in blood glucose after carbohydrate-rich meals.
That mechanism is intuitively appealing for people with type 2 diabetes, prediabetes, or large postprandial (after-meal) glucose spikes. Clinical research has tested single-meal challenges and longer supplementation periods, looking at postprandial glucose and insulin, fasting glucose, HbA1c, and related markers.
The honest summary up front: evidence is mixed and endpoint-dependent. The most consistent signal is a short-term reduction in postprandial glucose (and often insulin) when mulberry extract or DNJ-enriched powder is taken with carbohydrate. Effects on fasting glucose and HbA1c are weaker and inconsistent across systematic reviews—some pooled analyses report modest average improvements; others find no clear benefit on those longer-term markers. Study products, DNJ doses, durations, and baseline metabolic status vary widely. Mulberry extract is not a replacement for proven diabetes care.
This article walks through effectiveness, proposed mechanisms, clinical research, dosing used in trials, how mulberry stacks up against other popular glycemic adjuncts, safety, and practical FAQs—anchored to published PubMed-indexed sources.
Effectiveness
Postprandial glucose is where mulberry leaf / DNJ evidence is strongest:
- Phimarn and colleagues (2017) pooled randomized trials of Morus alba products and found significant reductions in postprandial glucose at 30, 60, and 90 minutes after carbohydrate challenges (mean differences about −1.04, −0.87, and −0.55 mmol/L, respectively). They did not find significant pooled effects on fasting blood sugar, HbA1c, or HOMA-IR, and they reported no serious adverse effects in the included trials.[1]
- Jeong, Jang, and Kim (2022) similarly concluded that Morus alba can reduce postprandial glucose and insulin, but judged the overall evidence insufficient to conclude that it is an effective intervention for lowering blood glucose more broadly; their quantitative synthesis did not support clear improvements in fasting glucose or HbA1c.[2]
Fasting glucose and HbA1c look more favorable in some newer poolings—but not all:
- Cui and colleagues (2023) meta-analyzed 12 clinical trials (615 participants) of mulberry leaf or mulberry leaf extract and reported weighted mean reductions in fasting blood glucose of about −0.47 mmol/L, HbA1c of about −2.92 mmol/mol (IFCC units; roughly on the order of a few tenths of a percent on the familiar NGSP % scale), and fasting plasma insulin of about −0.58 μIU/mL. Subgroup signals favored longer use (≥8 weeks) and participants who were not metabolically healthy or who had higher baseline fasting glucose.[3]
- Chen and colleagues (2022), pooling RCTs of mulberry consumption more broadly for cardiometabolic markers, reported a significant reduction in HbA1c (WMD about −0.55%) plus favorable shifts in several lipids and CRP, while other glycemic endpoints were less consistently improved versus control.[4]
Important caveats: Heterogeneity is often high; products range from whole-leaf powder to proprietary DNJ-standardized extracts; some “mulberry” trials include fruit or mixed preparations rather than leaf alone; and several longer RCTs that improve postprandial markers still fail to move HbA1c. Individual trials in people with impaired glucose metabolism have sometimes improved sensitive postprandial indicators without changing HbA1c or fasting glucose over 12 weeks.[5]
Bottom line on effectiveness: Mulberry leaf extract / DNJ most reliably blunts after-meal glucose (and often insulin) rises when taken with carbohydrate. Average effects on fasting glucose and HbA1c in meta-analyses are modest at best and contested across reviews. It should never replace lifestyle therapy or prescribed diabetes medicines.
Mechanism of Action
How might mulberry extract influence blood sugar? The best-supported pathway is intestinal carbohydrate-enzyme inhibition, led by DNJ and related iminosugars.
Asano and colleagues characterized polyhydroxylated alkaloids from Morus alba (and silkworms that feed on mulberry), including 1-deoxynojirimycin, a potent inhibitor of mammalian digestive glycosidases—supporting the idea that dietary DNJ can slow breakdown of starch and disaccharides in the small intestine.[6] Parida, Takasu, and Nakagawa’s comprehensive review of mulberry leaf iminosugars (DNJ, D-fagomine, and related compounds) summarizes production, pharmacokinetics, and metabolic health claims: DNJ’s α-glucosidase / sucrase inhibition delays carbohydrate digestion and glucose absorption, which aligns with clinical reductions in early postprandial glucose; the review also notes relatively rapid clearance and bioavailability considerations that may limit how long a single dose acts.[7]
This pharmacology is conceptually similar to prescription α-glucosidase inhibitors (e.g., acarbose), though mulberry products deliver far lower, food-supplement-level enzyme inhibition and are not regulated or dosed as drugs.
Additional phytochemicals in mulberry leaf (flavonoids, phenolics, polysaccharides) are often discussed as contributing to metabolic effects in mechanistic literature,[3] but DNJ-driven α-glucosidase inhibition remains the clearest clinical story for acute postprandial glucose lowering.
Important caveats:
- Mechanism evidence is strongest for meal-related glucose excursions, not for insulin secretion or hepatic glucose output the way metformin or GLP-1 agonists work.
- Low bioavailability and rapid clearance of DNJ may help explain why acute challenge studies look cleaner than long-term HbA1c outcomes.[7]
- Mulberry extract does not replace insulin or act like a sulfonylurea; any glucose-lowering effect after meals is primarily delayed carbohydrate absorption.
Clinical Research Results
Landmark and illustrative human studies
Kimura et al., 2007 (J Agric Food Chem). Healthy volunteers took DNJ-enriched mulberry powder providing 0, 6, 12, or 18 mg DNJ, then 50 g sucrose. The 0.8 g and 1.2 g powder doses (12 and 18 mg DNJ) significantly suppressed postprandial glucose and insulin elevations—an early dose-finding signal for food-grade DNJ enrichment.[8]
Mudra et al., 2007 (Diabetes Care). In a crossover design comparing type 2 diabetes and control volunteers, 1 g mulberry leaf extract with 75 g sucrose reduced the glucose response over 120 minutes versus placebo and increased breath hydrogen, consistent with carbohydrate malabsorption from disaccharidase inhibition.[9]
Asai et al., 2011 (J Diabetes Investig). Two complementary trials in adults with impaired fasting glucose: (1) single-dose crossover of mulberry extract providing 3, 6, or 9 mg DNJ with boiled white rice showed dose-dependent attenuation of postchallenge glycemia; (2) 12 weeks of 6 mg DNJ three times daily improved serum 1,5-anhydroglucitol (a marker sensitive to postprandial control) versus placebo, but FPG, HbA1c, and glycated albumin did not differ between groups.[5]
Kim et al., 2015 (J Med Food). In 36 adults with impaired fasting glucose, 5 g/day mulberry leaf aqueous extract for 4 weeks attenuated postprandial glucose, insulin, and C-peptide responses (notably at 30–60 minutes) and lowered insulin iAUC versus placebo.[10]
Lown et al., 2017 (PLoS One). In 37 normoglycemic adults, proprietary mulberry extract (Reducose®, standardized to ~5% DNJ) at 125 mg (≈6.75 mg DNJ), 250 mg (≈12.5 mg DNJ), and 500 mg (≈25 mg DNJ) with 50 g maltodextrin produced a classical dose–response reduction in glucose and insulin positive iAUC over 120 minutes (significant at 250 and 500 mg for glucose). Gastrointestinal symptom odds did not differ statistically from placebo across arms.[11]
Riche et al., 2017 (Complement Ther Med). Small pilot RCT in type 2 diabetes (n = 24 enrolled; 17 completers): 1,000 mg standardized MLE three times daily with meals for 3 months improved postprandial self-monitored glucose versus baseline and placebo, while HbA1c fell numerically (7.30% → 6.94%) without reaching significance versus placebo. Investigators also reported a ~15% rise in serum creatinine in the MLE arm versus baseline/placebo—an important safety signal in a small sample.[12]
Thaipitakwong et al., 2020 (Complement Ther Med). Dose-finding identified 12 mg DNJ as a minimum effective single dose for postprandial attenuation; a 12-week study in obese adults with borderline diabetes used 12 mg DNJ three times daily and reported small within-group reductions in FPG and HbA1c versus baseline, with common GI symptoms (bloating, flatulence, loose stools). Improvement in glucose tolerance testing was not observed.[13]
Wang et al., 2018 (Medicine). Exploratory crossover work found mulberry leaf extract reduced the glycemic indexes of several common dietary carbohydrates when co-ingested—again supporting a meal-timing, enzyme-inhibition use case.[14]
What systematic reviews conclude
Taken together: Phimarn and Jeong emphasize postprandial benefit with uncertain fasting/A1c effects,[1][2] while Cui and Chen report pooled reductions in fasting glucose and/or HbA1c that depend on inclusion criteria and preparation type.[3][4] Acute RCTs (Kimura, Mudra, Asai study 1, Lown, Wang) reinforce a dose-responsive, meal-adjacent glucose-blunting effect,[5][8][9][11][14] whereas longer trials often show mixed durability on HbA1c.[5][12][13] Heterogeneity in DNJ content, extract standardization, duration, and participant phenotype remains a major limit on applying any single “average effect” to every reader.
Dosing
There is no universally agreed therapeutic dose of mulberry leaf extract for blood sugar, and products are not dosed like prescription α-glucosidase inhibitors. What can be stated from trials:
| Context | Amounts appearing in research |
|---|---|
| DNJ single-challenge dose-finding | About 6–18 mg DNJ with sucrose or starch; stronger suppression often at ≥12 mg DNJ.[8][13] |
| Asai 2011 acute / chronic | 3–9 mg DNJ once with rice; chronic arm 6 mg DNJ three times daily for 12 weeks.[5] |
| Lown 2017 (Reducose® ~5% DNJ) | 125 / 250 / 500 mg extract (≈6.75 / 12.5 / 25 mg DNJ) with 50 g maltodextrin; significant glucose iAUC reduction at 250 and 500 mg.[11] |
| Thaipitakwong 2020 | 12 mg DNJ three times daily for 12 weeks in borderline diabetes.[13] |
| Kim 2015 | 5 g/day mulberry leaf aqueous extract for 4 weeks (DNJ content not the primary labeling focus of that report).[10] |
| Mudra 2007 | 1 g mulberry leaf extract with 75 g sucrose (acute).[9] |
| Riche 2017 | 1,000 mg standardized MLE three times daily with meals for 3 months.[12] |
Practical framing (not a prescription): Many commercial “blood sugar” mulberry products emphasize DNJ milligrams per serving (often on the order of the 6–25 mg DNJ range studied in challenge trials) and instruct use with carbohydrate-containing meals. Leaf-powder gram doses and proprietary extract milligram doses are not interchangeable without knowing DNJ standardization. Higher is not automatically better—GI effects of enzyme inhibition can increase with dose, as seen with pharmaceutical AGIs.[15]
Always confirm whether the label reports DNJ content, extract amount, or raw leaf powder; prefer third-party–tested products; and do not escalate dose on your own if you take insulin, sulfonylureas, or other glucose-lowering drugs.
Comparable Efficacy to Other Similar Treatments
Head-to-head RCTs comparing mulberry extract directly with other popular “blood sugar” supplements—or with prescription acarbose—are scarce. Comparisons below are indirect and should be read as context, not a ranking contest.
Acarbose / α-glucosidase inhibitors (drug class analogy). A Cochrane-based meta-analysis by van de Laar and colleagues found clear glycemic benefits of AGI monotherapy in type 2 diabetes (e.g., acarbose HbA1c reduction on the order of about −0.77% versus placebo), with characteristic GI side effects and no proven mortality benefit in that synthesis.[15] Mulberry DNJ shares a related enzyme-inhibition idea at supplement doses, but effect sizes, regulatory status, and evidence density are not equivalent to prescription AGIs.
*White kidney bean (Phaseolus vulgaris) extract. Proprietary α-amylase–inhibitor preparations have meta-analytic support mainly for modest weight / fat loss, not as a primary HbA1c therapy. Udani, Tan, and Molina (2018) pooled trials and reported average weight-loss differences of about −1.08 kg versus control contexts.[16] Mechanistically, white bean targets α-amylase (starch) while mulberry DNJ emphasizes α-glucosidase / sucrase*—overlapping “carb blocker” marketing, different primary enzymes and outcome literature.
Chromium. Suksomboon and colleagues’ diabetes meta-analysis reported pooled HbA1c and fasting-glucose reductions with chromium supplementation and adverse-event rates similar to placebo at usual trial doses—yet the broader chromium literature remains mixed on clinical meaningfulness.[17] Chromium’s proposed story is insulin-action potentiation; mulberry’s clearest story is intestinal enzyme delay. They are not interchangeable.
Berberine. A systematic review and meta-analysis of 14 randomized trials (1,068 participants) found berberine improved hyperglycemia and lipids versus lifestyle/placebo contexts and suggested additive glycemic benefit with some oral hypoglycemics; methodological quality was generally low.[18] Many evidence summaries discuss berberine’s glycemic signal as more frequently framed around fasting glucose/HbA1c than mulberry’s, while mulberry’s cleaner signal is often postprandial.
Honest comparative takeaway: Mulberry extract / DNJ is best framed as a meal-timed postprandial adjunct with mixed longer-term A1c data.[1–5][11] Prescription AGIs have stronger, drug-level glycemic evidence and more GI burden at therapeutic doses.[15] White kidney bean literature is weight-focused more than diabetes-endpoint-focused.[16] Chromium and berberine each have their own mixed-to-modest meta-analytic footprints via different mechanisms.[17][18] None of these supplements is a substitute for metformin, GLP-1 receptor agonists, SGLT2 inhibitors, insulin, or medical nutrition therapy when those are indicated.
Safety Profile
Adverse Effects
Short-term challenge studies and several RCTs generally report acceptable tolerability. Lown and colleagues found no statistically significant increase in odds of nausea, cramping, distension, or flatulence versus placebo across Reducose doses studied.[11] Phimarn’s meta-analysis likewise noted no serious adverse effects in included Morus alba trials.[1]
Gastrointestinal symptoms—bloating, flatulence, loose stools—are the most biologically expected adverse effects (carbohydrate that escapes digestion can ferment), and they were commonly noted in Thaipitakwong’s mulberry-leaf study.[13]
A dedicated 4-week safety RCT of green tea containing 550 mg MLE three times daily in healthy adults reported no adverse reactions attributable to the product and no difference in adverse-event incidence versus control beverage.[19]
Kidney signal caution: Riche’s small diabetes pilot observed a significant increase in serum creatinine with high-dose MLE (1,000 mg three times daily) versus baseline and placebo.[12] That finding is not proof of common nephrotoxicity, but it argues against unsupervised high-dose use—especially in people with reduced kidney function—and supports laboratory monitoring if a clinician agrees to a trial.
Drug Interactions
High-quality dedicated interaction trials are limited. Mechanistic caution is warranted because DNJ-related α-glucosidase inhibition can reduce/delay carbohydrate absorption:[6][7]
- Insulin and insulin secretagogues (e.g., sulfonylureas): Theoretical increased risk of hypoglycemia if postprandial glucose falls more than expected when mulberry is added to meals; glucose self-monitoring and clinician-guided medication adjustment are prudent.
- Other antidiabetes medicines (including metformin, GLP-1 RAs, SGLT2 inhibitors, and prescription AGIs such as acarbose): Additive glucose-lowering or overlapping GI effects are plausible—especially if combined with acarbose/miglitol—without assuming a fully characterized pharmacokinetic interaction. Do not stack enzyme inhibitors without professional advice.
- Medications requiring food for absorption or that are sensitive to GI transit: Formal mulberry-specific interaction data are sparse; separate counseling with a pharmacist is reasonable for complex regimens.
Precautions
- Not a disease treatment: Mulberry supplements are not FDA-approved to treat diabetes.
- Kidney disease: Given the creatinine signal in one pilot RCT,[12] people with CKD or rising creatinine should avoid self-directed high-dose MLE.
- Pregnancy and lactation: Adequate safety data for DNJ-standardized extracts at pharmacologic supplemental doses are insufficient for routine recommendation; do not self-prescribe for gestational diabetes.
- Carbohydrate-dependent timing: Benefits in trials generally require taking the product with the carbohydrate challenge/meal; dosing between meals is less aligned with the mechanism.
- Quality / standardization: DNJ content varies widely across commercial leaf products;[8] prefer clear DNJ labeling and reputable manufacturing.
- Surgery / glucose-lowering drugs: Disclose all supplements before procedures and medication changes.
FAQs
Q1. Can mulberry extract reverse type 2 diabetes?
No. The best-supported effect is blunting postprandial glucose rises; meta-analyses disagree on the strength of fasting glucose/HbA1c benefit.[1–4] Diabetes remission, when it occurs, is driven by comprehensive medical and lifestyle care—not mulberry alone.
Q2. Is DNJ-standardized extract better than plain mulberry leaf powder?
Many positive acute studies specifically used DNJ-enriched or DNJ-standardized preparations.[5][8][11] Gram doses of aqueous leaf extract have also shown postprandial benefits.[10] Comparability hinges on actual DNJ (and related iminosugar) delivery, which is poorly guaranteed by “mulberry leaf” labeling alone.[7][8]
Q3. Should I take it only with meals?
Yes—that matches both the α-glucosidase mechanism and the design of challenge RCTs.[5][8][9][11] Taking it away from carbohydrate is less likely to reproduce studied effects.
Q4. I already take metformin (or insulin). Can I add mulberry?
Only with clinician approval. Because the extract can lower postprandial glucose,[1][11][12] adding it without guidance could increase hypoglycemia risk or confuse interpretation of medication effects—especially with insulin or sulfonylureas.
Q5. How is this different from white kidney bean “carb blockers”?
White kidney bean extracts mainly inhibit α-amylase and have meta-analytic data centered on modest weight/fat loss.[16] Mulberry DNJ is better known for α-glucosidase / sucrase inhibition and postprandial glucose trials.[6][7] Marketing overlap does not mean equal evidence for A1c lowering.
Q6. Who is least likely to benefit?
People expecting large fasting-glucose or HbA1c changes from mulberry alone may be disappointed—several reviews and longer RCTs find weak or null effects on those endpoints despite postprandial improvements.[1][2][5] Very low-carbohydrate meals also leave less substrate for an α-glucosidase–based effect.
Conclusion
Mulberry leaf extract sits at the intersection of a clear mechanistic story and uneven long-term clinical proof. DNJ and related iminosugars inhibit intestinal carbohydrate-digesting enzymes,[6][7] and multiple RCTs plus meta-analyses support lower postprandial glucose (and often insulin) when extract is taken with carbohydrate.[1][2][5][8–11][14] Pooled effects on fasting glucose and HbA1c are modest and inconsistent across systematic reviews,[1–4] and at least one longer impaired-glucose trial improved a postprandial marker without changing HbA1c.[5]
If mulberry extract is considered at all, the evidence-aligned posture is:
- Treat it as an optional, meal-timed adjunct, never a substitute for medical therapy.
- Prefer products and doses in the range actually studied—often about 6–25 mg DNJ per carbohydrate-containing meal, or other regimens with documented composition (e.g., specific gram doses of leaf extract).[5][8][10–13]
- Monitor glucose closely if you use insulin or other glucose-lowering drugs.
- Respect GI effects and the limited but non-zero kidney caution from high-dose pilot data.[12][13]
For many readers, the highest-yield next steps remain the unglamorous ones: nutrition quality (including carbohydrate quality and portioning), physical activity, sleep, weight management when appropriate, and evidence-based medications. Mulberry extract may be a footnote in that plan for selected adults interested in postprandial control—not the headline.
References
- Phimarn W, Wichaiyo K, Silpsavikul K, Sungthong B, Saramunee K. A meta-analysis of efficacy of Morus alba Linn. to improve blood glucose and lipid profile. Eur J Nutr. 2017;56(4):1509-1521. PMID: 26972284.
- Jeong HI, Jang S, Kim KH. Morus alba L. for Blood Sugar Management: A Systematic Review and Meta-Analysis. Evid Based Complement Alternat Med. 2022;2022:9282154. PMID: 35656460.
- Cui W, Luo K, Xiao Q, et al. Effect of mulberry leaf or mulberry leaf extract on glycemic traits: a systematic review and meta-analysis. Food Funct. 2023;14(3):1277-1289. PMID: 36644880.
- Chen X, Sohouli MH, Nateghi M, Melekoglu E, Fatahi S. Impact of mulberry consumption on cardiometabolic risk factors: A systematic review and meta-analysis of randomized-controlled trials. J Clin Pharm Ther. 2022;47(12):1982-1993. PMID: 36509962.
- Asai A, Nakagawa K, Higuchi O, et al. Effect of mulberry leaf extract with enriched 1-deoxynojirimycin content on postprandial glycemic control in subjects with impaired glucose metabolism. J Diabetes Investig. 2011;2(4):318-323. PMID: 24843505.
- Asano N, Yamashita T, Yasuda K, et al. Polyhydroxylated alkaloids isolated from mulberry trees (Morus alba L.) and silkworms (Bombyx mori L.). J Agric Food Chem. 2001;49(9):4208-4213. PMID: 11559112.
- Parida IS, Takasu S, Nakagawa K. A comprehensive review on the production, pharmacokinetics and health benefits of mulberry leaf iminosugars: Main focus on 1-deoxynojirimycin, d-fagomine, and 2-O-ɑ-d-galactopyranosyl-DNJ. Crit Rev Food Sci Nutr. 2023;63(19):3468-3496. PMID: 34658276.
- Kimura T, Nakagawa K, Kubota H, et al. Food-grade mulberry powder enriched with 1-deoxynojirimycin suppresses the elevation of postprandial blood glucose in humans. J Agric Food Chem. 2007;55(14):5869-5874. PMID: 17555327.
- Mudra M, Ercan-Fang N, Zhong L, Furne J, Levitt M. Influence of mulberry leaf extract on the blood glucose and breath hydrogen response to ingestion of 75 g sucrose by type 2 diabetic and control subjects. Diabetes Care. 2007;30(5):1272-1274. PMID: 17303787.
- Kim JY, Ok HM, Kim J, Park SW, Kwon SW, Kwon O. Mulberry leaf extract improves postprandial glucose response in prediabetic subjects: a randomized, double-blind placebo-controlled trial. J Med Food. 2015;18(3):306-313. PMID: 25343729.
- Lown M, Fuller R, Lightowler H, et al. Mulberry-extract improves glucose tolerance and decreases insulin concentrations in normoglycaemic adults: Results of a randomised double-blind placebo-controlled study. PLoS One. 2017;12(2):e0172239. PMID: 28225835.
- Riche DM, Riche KD, East HE, Barrett EK, May WL. Impact of mulberry leaf extract on type 2 diabetes (Mul-DM): A randomized, placebo-controlled pilot study. Complement Ther Med. 2017;32:105-108. PMID: 28619294.
- Thaipitakwong T, Supasyndh O, Rasmi Y, Aramwit P. A randomized controlled study of dose-finding, efficacy, and safety of mulberry leaves on glycemic profiles in obese persons with borderline diabetes. Complement Ther Med. 2020;49:102292. PMID: 32147046.
- Wang R, Li Y, Mu W, et al. Mulberry leaf extract reduces the glycemic indexes of four common dietary carbohydrates. Medicine (Baltimore). 2018;97(34):e11996. PMID: 30142838.
- van de Laar FA, Lucassen PL, Akkermans RP, van de Lisdonk EH, Rutten GE, van Weel C. Alpha-glucosidase inhibitors for patients with type 2 diabetes: results from a Cochrane systematic review and meta-analysis. Diabetes Care. 2005;28(1):154-163. PMID: 15616251.
- Udani J, Tan O, Molina J. Systematic Review and Meta-Analysis of a Proprietary Alpha-Amylase Inhibitor from White Bean (Phaseolus vulgaris L.) on Weight and Fat Loss in Humans. Foods. 2018;7(4):63. PMID: 29677119.
- Suksomboon N, Poolsup N, Yuwanakorn A. Systematic review and meta-analysis of the efficacy and safety of chromium supplementation in diabetes. J Clin Pharm Ther. 2014;39(3):292-306. PMID: 24635480.
- Dong H, Wang N, Zhao L, Lu F. Berberine in the treatment of type 2 diabetes mellitus: a systemic review and meta-analysis. Evid Based Complement Alternat Med. 2012;2012:591654. PMID: 23118793.
- Yasumoto K, Hoshiko H, Sekiguchi N, Obata H, Takara T. Safety evaluation of a beverage containing mulberry leaf extract. Biosci Biotechnol Biochem. 2022;86(4):519-527. PMID: 35089999.