Systematic Reviews
Copyright ©The Author(s) 2019.
World J Diabetes. Feb 15, 2019; 10(2): 96-113
Published online Feb 15, 2019. doi: 10.4239/wjd.v10.i2.96
Table 3 Animal and in vitro trials examining effects of long-term royal jelly treatment
Ref.Study designSubjectsTreatmentOutcome measuresEffectiveness
Ghanbari et al[14]Randomized controlled trialN = 8 healthy male Wistar rats aged 10-12 wk (control)100 mg/kg BW royal jelly dissolved in 1 mL of water daily for 6 wkHyperinsulinemia: ELISA test on plasma sampleTreatment significantly improved insulin levels (d = 1.67) and hyperglycemic fasting blood glucose (d = -2.72) levels to levels similar to healthy control group
N = 8 diabetic male Wistar rats aged 10-12 wkHyperglycemia: Fasting plasma glucose
N = 8 healthy male Wistar rats aged 10-12 wk receiving treatment
N = 8 diabetic male Wistar rats aged 10-12 wk receiving treatment
Fujii et al[32]Controlled trialN = 80 male streptozotocin-diabetic rats aged 5 wk equally split into three experimental groups and one control groupEach experimental group had one of 1, 10, and 100 mg/kg body weight royal jelly administered orally by force for 4 wk. Control group received purified waterHyperglycemia: Blood glucose (unknown whether fasting)Royal jelly administration overall slightly decreased blood glucose levels in non-dose dependent manner (no information on statistical significance)
Body weightNo significant change in body weight between groups
Membrez et al[33]Randomized controlled trialN = 15 male db/db mice aged 6-8 wk in control group1 g/kg body weight of sebacic acid was added to chow food in one experimental group, and 10 g/kg body weight SA to second experimental group’s chow for 6 wkHyperglycemia: OGTT and fasting (plasma samples)In more heavily supplemented group: Hyperglycemia significantly improved (d = -1.86) and improved glucose clearance (d = -3.20), HbA1c significantly decreased (d = -1.89), ketone bodies significantly increased (d = 1.16), dose response relationship observed, gluconeogenic and lipogenic enzyme expression significantly decreased (insufficient information for SMD estimation), food intake was significantly decreased (d = -1.82).
N = 30 male db/db mice aged 6-8 wk equally split in two experimental groupsHbA1c: Plasma samples
Liver gene expression: RNA extracted from liver samples
Food intake: Chow consumed
Takikawa et al[7]In vitroL6 myotubes grown in cell culture and collected from healthy male mice 7 wk of ageCell cultured myotubes treated with 10H2DAGlucose clearance: GLUT4 translocation to plasma membraneSignificantly improved GLUT4 translocation to plasma membrane in skeletal muscle cells compared to non-treated myotube cells (d = 0.4698)
Mice fed 1.6 mmol/kg 10H2DA
Yoneshiro et al[34]Controlled trialN = 8 3-wk old healthy male mice (control)High fat diet with 5% lyophilized royal jelly powder for 17 wkBody weight gainBody weight gain due to white adipose tissue significantly reduced compared to HFD group (d = -2.82)
N = 11 3-wk old healthy male mice fed HFDHyperlipidemia: Plasma sampleSignificantly decreased levels of NEFA compared to HFD (d = -1.6072)
N = 11 3-wk old healthy male mice fed high fat diet with treatmentHyperglycemia: Plasma sampleSignificantly improved hyperglycemia compared to HFD group (d = -2.04)
Insulin resistance: HOMA-IRHOMA-IR significantly decreased compared to HFD group, not significantly different from control group (d = -1.23)
Zamami et al[15]Controlled trialN = 6 6-wk old healthy male Wistar rats (control, received water)Two experimental groups: One fed 100 mg/kg and the other 300 mg/kg of dilute enzymatically treated royal jelly supplementation daily for 8 wkInsulin resistance: HOMA-IRHigh fructose diet induced insulin resistance in rats
N = 5 6-wk old healthy male Wistar rats as vehicle-treated group (received high fructose consumption)Food intakePlasma insulin levels and HOMA-IR similar between healthy control group and fructose drinking rats supplemented with 300 mg/kg royal jelly. Dose dependent relationship observed d = -0.7063 (effect size of 300 mg/kg royal jelly on fructose drinking rats)
N = 6 + 6 6-wk old healthy male Wistar rats (received high fructose consumption) in two treatment groupsBody weightNo significant difference in body weight and FBG between groups
Plasma triglyceridesPlasma triglycerides significantly decreased compared to control dose-dependently (d = -1.62)
Watadani et al[35]Controlled trialN = 7 female KK-Ay mice 5 wk of age in control group3 mg/kg 10H2DA for 4 wkHyperglycemia: Plasma glucose samples collected in intervals after OGTTSignificantly improved glucose clearance (d = -1.33) and fasting blood glucose (d = -1.23)
N = 8 female KK-Ay mice 5 wk of age in treatment groupBody weight: Adiposity index of abdominal, mesenteric and retroperitoneal fat tissueBody weight did not differ between groups
Insulin resistance: HOMA-IRSignificantly improved insulin sensitivity (d = -4.44)
Glucose regulatory proteins: AMPK, G6Pase, Pck1 levels, GLUT4, GS/GSK in tissue homogenatesSignificantly increased levels of G6Pase (d = 1.22) and Pck1(d = 0.77) mRNA in liver cells. Significantly increased levels of pAMPK in muscle (d = 3.13), but no change in liver. Insignificant increase in GLUT4 in muscle cells. No change in GS/GSK levels between groups
Yoshida et al[36]Controlled trial16 female KK-Ay mice split into control and experimental groups10 mg/kg royal jelly in 1/15M phosphate buffer 5 d/wk for 4 wkSignificantly improved rates of glucose clearance (d = -1.25)
Insignificantly decreased body weight
Significantly increased pAMPK levels in liver (d = 2.39) and skeletal muscle (d = 1.73). Significantly decreased G6Pase mRNA levels in liver (d = -1.65), but no change in Pck mRNA levels. Insignificantly increased GLUT4 levels in skeletal muscle
Significantly decreased plasma NEFA (d = -1.42). No change in plasma TG
No significant change in plasma insulin