Table 1.
Effect of curcumin on obesity in human, animal and in vitro studies. An explanation of the abbreviations can be found at the end of the review.
| Type of Study | Experimental Design and Treatments | Results | Trial Lenght | Ref. |
|---|---|---|---|---|
| Human study | Randomized, controlled trial; 44 obese subjects supplemented with curcumin complexed with phosphatidylserine in phytosome form |
↑BW loss ↑Enhance body fat reduction ↑Waistline reduction ↑Hip circumference reduction ↓BMI |
30 days | [105] |
| Human study | Randomized, double-blind, crossover trial; 30 obese individuals supplemented with capsules containing 500 mg curcuminoids plus 5mg bioperine; two capsules per day |
↓Serum IL1β and IL-4 levels | 4 weeks | [106] |
| Human study | Randomized, double-blind, placebo-controlled crossover trial; 30 obese individuals supplemented with capsules containing 500 mg curcuminoids plus 5 mg bioperine; one capsule per day |
↓Serum triglycerides level | 30 days | [107] |
| Human study | Randomized, doubled-blinded, placebo-controlled, crossover design, 62 overweight/obese females with systemic inflammation supplemented with turmeric; 800 mg per day |
No significant changes in none of the investigated metabolic parameters or inflammation |
10 weeks | [108] |
| Human study | Randomized, double-blinded, placebo-controlled trial. Elderly (n = 36, N 50 years); placebo group, 1 g per day curcumin group and 4 g per day curcumin group |
↔Serum lipid profile (triglycerides, total, LDL-C, HDL-C) | 6 months | [109] |
| Human study | A pre–post study. Healthy adults (n = 8, 43–70 years) received 10 mg per day |
↓Serum LDL, Apo B, Apo B/Apo A ↑Serum HDL and Apo A |
30 days | [110] |
| Animal study | Male Sprague–Dawley rats in an HFD-induced obesity model; control group, curcumin 100 mg/kg/BW per daygroup, 400 mg/kg/BW per day, HFD group, HFD + curcumin 100 or HFD + curcumin 400 | ↓Liver triglYcerydes ↓Serum fetuin-A |
8 weeks | [111] |
| Animal study | Male C57BL/6 J mice (8 weeks old) in an HFD-induced obesity and insulin resistance model; LFD group, HFD group and HFD + curcumin group—50 mg/kg BW by gavage | ↔BW ↑NrF2 in skeletal muscle ↑Glucose disposal and insulin sensitivity ↓MDA and ROS in skeletal muscle and mitochondria |
15 days | [112] |
| Animal study | Male C57BL/6 J mice (5 weeks old) in an HFD-induced obesity model; LFD group, HFD group or HFD + curcumin (4 g/kg diet, added 2 days/week) group |
↓BW and fat ↓NF-κB ↓SREBP-1c ↔Wnt signaling in mature adipocytes ↓Inflammatory in adipocytes |
28 weeks | [113] |
| Animal study | European obese cats (6.5 years old); control group, citrus group or curcumin group | ↓IFN-γ and IL-2 mRNA levels ↔mRNA expression of TNF-α, IL-1β, IL-4, IL-5, IL-10, IL-12, IL-18, TGF-β |
8 weeks | [114] |
| Animal study | Male C57BL/6 J, ob/ob mice and nonobese littermates in a model of steatosis; ob/ob control group, lipo group, ob/ob. + curcumin group, nonobese control group or nonobese + curcumin group |
↓NF-κB pathway ↓TNF ↓IL-6 ↑ IL-4 ↑Insulin sensitivity ↑Serum adiponectin |
24 or 72 h | [115] |
| Animal study | Male C57BL/6 mice (4 weeks old) in an HFD-induced obesity model; control group, HFD group or HFD + curcumin group (500 mg/kg of diet) | ↓BW, fat, microvessel density in adipose tissue. ↓Liver weights and hepatic steatosis ↓Serum glucose and triglycerides ↑Fatty acid and energy metabolism (↑ P-AMPK, P-ACC mRNA expression; ↓PPARγ and C/EBPα mRNA expression) |
12 weeks | [116] |
| Animal study | Male Wistar rats (100–120 g) in an HFD-induced obesity model; control group, HFD control group, HFD + 30 mg/kg BW curcuminoid group, HFD + 60 mg/kg BW curcuminoid group, HFD + 90 mg/kg BW curcuminoid group | ↓Plasma FFA ↓glucose levels |
12 weeks | [117] |
| Animal study | Male Golden-Syrian hamsters (4 weeks old) in an HFD-induced obesity model; HFD group or HFD + curcumin (0.05% in diet) | ↔BW, food intake, fat pad mass, plasma glucose Plasma FFA, triglycerydes, leptin, insulin ↑Plasma HDL-C, Apo A-I ↓Hepatic cholesterol and triglycerydes ↑FA β-oxidation activity ↓FAS, HMG-CoA reductase ↓Lipid peroxide levels |
10 weeks | [118] |
| Animal study | Male wild-type C57BL/6 J mice (8–10 weeks old) in a diet-induced-obesity (DIO) model. Male ob/ob C57BL/6 J mice (3–5 weeks old); groups including DIO control group, DIO + 3% curcumin, ob/ob control group or ob/ob. + 3% curcumin |
↓BW and body fat ↑Glycemic status and insulin sensitivity ↓Adipose, hepatic and systemic inflammation ↑mRNA expression of adiponectin ↓Hepatic NF-κB activity |
60 days | [119] |
| Animal study | Male Sprague–Dawley rats in an HF-diet-induced obesity model; control group, high curcumin (5.00 g/kg BW, HFD group, HFD + low curcumin (1.25 g/kg diet) group or HFD + high curcumin (5.00 g/kg diet) group |
↓BW, blood glucose, insulin, leptin, TNF-α ↓Insulin resistance and leptin resistance |
4 weeks | [120] |
| In vitro study | 3T3-L1 cells treated with curcumin (0–30 μM) | ↑Apoptosis at 30 μM ↓Glycerol release ↓MAPK phosphorylation |
2 and 24 h | [121] |
| In vitro study | Primary cell culture from epididymal fat pads treated with curcumin (0–20 μM) | ↔Wnt signaling ↓Inflammatory and oxidative pathway ↓NF-κB signaling |
0–60 min | [113] |
| In vitro study | 3T3-L1 cells treated with curcumin (0–100 μM) | ↓ Adipocyte differentiation and lipid accumulation ↓FAS, PPARγ |
0–8 days | [122] |
| In vitro study | Rabbit subcutaneous adipocytes treated with curcumin (0–20 μg/mL) | ↑Cholesterol efflux from adipocytes ↑PPARγ, LXRα, ABCA1 |
24 h | [123] |
| In vitro study | 3T3-L1 cells treated with curcumin (0–30 μM) | ↓Adipocyte differentiation and fat accumulation ↓Cell viability ↓C/EBPβ, PPARγ and C/EBPα |
18, 24 and 48 h, 6 days | [77] |
| In vitro study | 3T3-L1 cells treated with curcumin (0–50 μM) for | ↑AMPK PPARγ ↑Phosphorylation of ACC ↓Fat accumulation |
8 days | [124] |
| In vitro study | 3T3-L1 cells treated with curcumin (0, 5,10 and 20 μM) | ↓Adipocyte differentiation, fat accumulation and adipogenesis ↑fat oxidation ↓ACC ↑AMPK activation ↑Apoptosis |
24 h | [116] |