60 diabetic rats divided into 6 groups:

• Distilled water,
• Honey,
• Glibenclamide,
• Glibenclamide and honey,
• Metformin, and
• Metformin and honey

Distilled water, honey, glibenclamide, glibenclamide and honey, metformin, or metformin and honey were administered orally once daily for 4 weeks.

Honey significantly increased insulin (0.41 ± 0.06 ng/mL), decreased blood glucose (12.3 ± 3.1 mmol/L), and reduced fructosamine (304.5 ± 10.1 µmol/L). Glibenclamide and metformin alone reduced blood glucose, but when combined with honey, blood glucose was significantly lower (3.3 ± 2.98 mmol/L) compared to glibenclamide (13.9 ± 3.4 mmol/L) or metformin alone (13.2 ± 2.9 mmol/L).

Diabetic rats (6 rats/group) induced with streptozotocin (STZ) at a dose of 60 mg/kg.

Distilled water (0.5 mL/day)

Honey (0.2 g/kg/day, 1.2 g/kg/day, and 2.4 g/kg/day) by gavage for 4 weeks.

In diabetic rats, total antioxidant status (TAS), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione-S-transferase (GST) activities were significantly reduced in the kidneys, while superoxide dismutase (SOD) activity was upregulated. Lipid peroxidation (TBARS) and fasting plasma glucose (FPG) were significantly increased, and body weight was decreased. Honey significantly increased body weight, TAS, and the activities of CAT, GPx, GR, and GST in diabetic rats.

Adult male Sprague-Dawley rats. Diabetes induced by STZ (60 mg/kg body weight).

Tualang honey (1.0 g/kg body weight).

Tualang honey supplementation in diabetic rats increased AST and ALT levels and also exerted a hepatoprotective effect in STZ-induced diabetic rats.

6 groups of 6 rats/group.

• Control rats fed standard pellet diet and water.
• Diabetic rats as untreated diabetic control.
• Diabetic rats treated with honey 1.0 g/kg BW for 21 days.
• Hypercholesterolemic rats: cholesterol (1.5%) and cholic acid (0.5%) mixed with diet.
• Hypercholesterolemic rats treated with honey (1.0 g/kg BW for 21 days).
• Diabetic rats treated with glibenclamide (0.5 mg/kg).

Honey treatment significantly reduced blood glucose levels in diabetic rats. Total Cholesterol (TC), Triglycerides (TG), Low-Density Lipoprotein (LDL), and Very Low-Density Lipoprotein (VLDL) were significantly decreased while High-Density Lipoprotein (HDL) was significantly increased. Alanine Aminotransferase (ALT, formerly SGPT), Aspartate Aminotransferase (AST, formerly SGOT), and C-Reactive Protein (CRP) were significantly reduced.

8 groups of diabetic rats (5-7 animals/group).

Treatments/Groups:

1. Distilled water (0.5 mL);
2. Honey (1.0 g/kg);
3. Metformin (100 mg/kg);
4. Metformin and honey;
5. Glibenclamide (0.6 mg/kg);
6. Glibenclamide and honey;
7. Metformin and glibenclamide; and
8. Metformin, glibenclamide, and honey orally, once daily for 4 weeks.

In diabetic kidneys, malondialdehyde (MDA) levels, glutathione peroxidase (GPx), and superoxide dismutase (SOD) activities were significantly increased, while catalase (CAT) activity, total antioxidant status (TAS), reduced glutathione (GSH), and the GSH:oxidized glutathione (GSSG) ratio were significantly decreased. CAT, glutathione reductase (GR), TAS, and GSH were significantly reduced in diabetic rats treated with metformin and/or glibenclamide alone. Conversely, metformin or glibenclamide combined with honey significantly increased CAT, GR, TAS, and GSH.

Diabetic rats (2 groups) and non-diabetic rats (2 groups).

Diabetic rats received distilled water (0.5 mL/day) or Tualang honey (1.0 g/kg/day). Non-diabetic rats also received distilled water (0.5 mL/day) or Tualang honey (1.0 g/kg/day).

Honey-treated diabetic rats had significantly reduced blood glucose levels [median (interquartile range) 8.8 (8.5) mmol/L] compared to diabetic control rats [17.9 (2.6) mmol/L].

8 groups of rabbits (6 animals/group); Groups I to IV were normal and healthy (non-diabetic), and Groups V to VIII were diabetic, induced by alloxan monohydrate.

Group I: Control group received 20 mL water orally. Groups II-IV orally received 5, 10, and 15 mg/kg BW honey, diluted with 20 mL/kg distilled water. Groups V-VI were treated with tolbutamide (250 mg and 500 mg). Group V: Diabetic control, treated with 20 mL water. Groups VI-VIII were orally treated with 5, 10, and 15 mL/kg honey, diluted to 20 mL with distilled water.

Oral administration of pure honey at a dose of 5 mL/kg did not significantly (P>0.05) increase glucose levels in alloxan-diabetic rabbits, whereas artificial honey, even at this low dose, increased blood glucose levels in normal rabbits.

48 adult male Wistar rats were divided into 6 groups.

Group 1a: Control, fed standard rat chow for 3 weeks. Group 1b: Fed honey with standard rat chow for 3 weeks. Group 2a: Alloxan-induced diabetes, fed standard rat chow for 3 weeks. Group 2b: Alloxan-induced diabetes, fed honey with standard rat chow for 3 weeks. Group 3a: Fed standard rat chow supplemented with fructose for 3 weeks. Group 3b: Fed standard rat chow supplemented with fructose and honey for 3 weeks.

(Rat chow = complete diet throughout life)

At the end of three weeks, daily honey consumption for 3 weeks was found to gradually and effectively reduce blood glucose levels in alloxan-induced diabetic rats. Honey also reduced hyperglycemia caused by long-term fructose consumption, although to a lesser extent than its effect on alloxan-induced hyperglycemia. Honey could not reduce blood glucose levels in control rats (neither alloxan-treated nor fructose-fed), even though it caused an increase in body weight, regardless of other substances administered simultaneously to the rats.

40 six-week-old Sprague-Dawley rats.

A powdered diet which was either sugar-free, or contained 8% sucrose, or 8% mixed sugars (simulating honey), or 10% honey, for 6 weeks.

HbA1c and triglyceride levels were significantly higher in all sugar-treated groups compared to rats fed the sugar-free diet.

55 Sprague-Dawley rats, approximately 8 weeks old.

3 experimental diets were prepared: sugar-free, 7.9% sucrose, or 10% honey.

Weight gain in honey-fed rats was significantly reduced compared to the sucrose-based diet. However, a significant finding was that honey consumption increased HDL cholesterol levels. A strong relationship has been observed between low HDL cholesterol levels and increased risk of cardiovascular diseases.

36 rats divided into 6 groups of 6 animals. Diabetes induced by STZ (60 mg/kg; IP).

Diabetic rats received distilled water (0.5 mL/day), honey (1.0 g/kg/day), metformin (100 mg/kg/day), or a combination of metformin (100 mg/kg/day) and honey (1.0 g/kg/day) orally for four weeks. Similarly, two groups of non-diabetic rats received distilled water (0.5 mL/day) or honey (1.0 g/kg/day).

Honey significantly increased GSH, TAS, and CAT and GR activities in diabetic rats, while FPG, MDA levels, and SOD activity were decreased.

The final results indicate that honey has a hypoglycemic effect and improves renal oxidative stress.

17 individuals (control group)

38 individuals (test group)

70 g sucrose daily for 30 days in the control group and 70 g honey daily for 30 days in the test group.

In healthy individuals, honey caused a slight decrease in body weight (1.3%) and body fat (1.1%), and reduced total cholesterol (3%), LDL-C (5.8%), triglycerides (11%), Fasting Blood Glucose (FBG) (4.2%), and C-Reactive Protein (CRP) (3.2%), while HDL-C (3.3%) increased. In patients (with hyperlipidemia), honey led to a 3.3% reduction in total cholesterol, 4.3% in LDL-C, 19% in triglycerides, and 3.3% in CRP.

48 patients with Type II diabetes:

• Honey group
• Control group

Honey group received escalating doses: 1 g/kg body weight/day for 2 weeks; then 1.5 g/kg body weight/day for the next 2 weeks; then 2 g/kg body weight/day for the following 2 weeks; and finally 2.5 g/kg body weight/day for the last 2 weeks.

In the honey group, body weight, total cholesterol, low-density lipoprotein cholesterol, and triglycerides decreased, while high-density lipoprotein cholesterol significantly increased. Hemoglobin A1c (HbA1c) levels significantly increased in the honey group.

24 healthy individuals, 16 individuals with Type II diabetes, 6 patients with hypertension.

12 healthy individuals inhaled distilled water vapor for 10 minutes. After a one-week washout, they inhaled honey solution (60% w/v) for 10 minutes. A separate group of 12 healthy individuals inhaled 10% dextrose solution for 10 minutes.

Honey inhalation significantly reduced random blood glucose levels from 199 ± 40.9 mg/dL to 156 ± 52.3 mg/dL after 30 minutes in (presumably healthy) individuals. Fasting blood glucose levels decreased over the 3 hours post-inhalation of honey, with the decrease being significant at 3 hours. In patients (with Type II diabetes or hypertension), blood glucose levels during a glucose tolerance test were significantly reduced after honey inhalation.

32 patients with Type II diabetes (non-insulin dependent).

Dietary intake of single test meals: 25 g glucose, fructose, or lactose; or 30 g honey; 50 g white bread; 125 g white rice; or apples (amount not specified in summary); and 150 g or 260 g of carrots.

Blood glucose and plasma insulin levels were measured at baseline and then at 15, 30, 60, 90, and 120 minutes postprandially. Taking the glycemic increase after glucose as 100%, the relative glycemic responses for other carbohydrates were: fructose, 81.3%; lactose, 68.6%; apples, 46.9%; potatoes, 41.4%; bread, 36.3%; rice, 33.8%; honey, 32.4%; and carrots, 16.1%. (Note: Potatoes were not listed in the treatment design summary).

20 young patients with Type I diabetes (test group).

10 healthy non-diabetic individuals (control group).

Calculated amounts of glucose, sucrose, and honey (dose = subject's weight in kg × 1.75, up to a maximum of 75 g per subject).

Honey, compared to sucrose, had a lower Glycemic Index (GI) and Peak Incremental Index (PII) in both patient and control groups. In the patient group, the increase in C-peptide levels after honey consumption was not significant compared to that after glucose or sucrose.

30 individuals with a confirmed family history (mother or father) of Type 2 diabetes.

Dietary challenge of glucose versus honey.

Plasma glucose levels in response to honey peaked at 30-60 minutes and showed a more rapid decline compared to glucose. Significantly, high tolerance for honey was also noted in these individuals (at risk for diabetes), indicating a lower glycemic index for honey.

48 individuals: healthy subjects and diabetic patients with dyslipidemia.

Various protocols included:

• Dextrose solution (250 mL water with 75 g dextrose) vs. honey solution (250 mL water with 75 g natural honey).
• Dextrose, honey, or artificial honey (250 mL water with 35 g dextrose + 40 g fructose).
• Honey solution daily for 15 days.
• Honey vs. artificial honey.
• 70 g dextrose vs. 90 g honey in Type 2 diabetic patients.
• 30 g sucrose vs. 30 g honey in diabetic patients.

Healthy individuals: Dextrose increased plasma glucose levels (PGL) at 1 and 2 hours, decreasing PGL after 3 hours. Honey increased PGL at 1 hour, decreasing it after 3 hours. Insulin and C-peptide increase after dextrose was significantly higher than after honey. Dextrose decreased total cholesterol and LDL-C at 1 hour (significant at 2 hours) and increased triglycerides (TG) at 1, 2, and 3 hours. Artificial honey transiently reduced cholesterol and LDL-C while increasing TG. Natural honey reduced cholesterol, LDL-C, and TG, while transiently increasing HDL-C. 15-day honey consumption reduced cholesterol, LDL-C, TG, CRP, homocysteine, and PGL, but increased HDL-C.

Patients with hypertriglyceridemia: Artificial honey increased TG; natural honey decreased TG. Dyslipidemic patients: Artificial honey increased LDL-C; natural honey decreased LDL-C. After 15 days, natural honey reduced cholesterol, LDL-C, and CRP.

Diabetic patients: Honey significantly increased PGL compared to dextrose. The PGL increase after honey was greater than after sucrose at 30 minutes, but less than after sucrose at other intervals. Compared to sucrose, honey elicited a greater insulin response at various intervals and increased PGL in diabetic patients.

20 adult diabetic volunteers with metabolic disorders, aged 30 to 65 years, of both sexes.

Honey dose: 2 g/kg body weight/day, administered as:

1. 50 mL (approx. 60 g) of honey dissolved in water (1:3 ratio), given twice daily before meals.
2. Remaining daily amount (approx. 25 mL or 30 g, depending on total daily dose) used for sweetening purposes.

Honey consumption led to greater increases in blood glucose levels in these patients but without inducing diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS). Long-term honey consumption also resulted in weight loss in all patients and improved blood pressure control in those with pre-existing hypertension. Cardiovascular status improved in patients with pre-intervention coronary heart disease (CHD).

50 patients with Type I diabetes.

30 non-diabetic controls.

Honey dose: 1.75 g/kg body weight.

Dextrose dose: 1.75 g dextrose/kg body weight.

The GI and PII values for a specific sweetener (sucrose or honey) did not show significant differences when comparing diabetic patients to controls. However, honey's GI and PII were significantly lower than those of sucrose in both patient and control groups. In both diabetic patients and controls, the increase in C-peptide levels after honey consumption was significant compared to that after glucose or sucrose.