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Table 1 Studies on the association between the Ucp1 polymorphisms and CMDs or CMD risk factors in different populations

From: Association of uncoupling protein (Ucp) gene polymorphisms with cardiometabolic diseases

SNP(s) Population and participants Association Allele/genotype frequencies Reference
+/− Condition
A–3826G Australian: overweight/obese F = 526 + ↑ BMI (P = 0.02), ↑ insulin (P = 0.03, not adjusted), and ↑ fasting glucose concentrations (P = 0.01, adjusted for BMI) G allele: 0.23 (Heilbronn et al. 2000)
A–3826G Brazil: T2D patients N = 981 and controls N = 534 T2D (P > 0.05) AA: 49.9%, AG: 37.7%, GG: 12.4%,
G allele: 0.313 in diabetics;
AA: 49.3%, AG: 39.5%, GG: 11.2%,
G allele: 0.310 in controls
(de Souza et al. 2013)
A–3826G Canadian: parents N = 123 and offsprings N = 138 from 64 families Body fat, RMR, and absolute changes in body fat over a 12-year period G allele: 0.28 (Oppert et al. 1994)
+ ↑ body fat gain over time (P < 0.05)
A–3826G Chinese: T2D patients N = 792, including DR group: PDR N = 220 and NPDR N = 228;
DNR group: N = 334
+ ↑ risk of PDR (additive model OR = 1.72, 95% CI: 1.06–2.79, P = 0.03) AA: 20.7%, AG: 49.3%, GG: 30.0%,
G allele: 54.6% in PDR group;
AA: 28.1%, AG: 48.2%, GG: 23.7%,
G allele: 47.8% in DNR group
(Zhang et al. 2015)
+ PDR (OR = 1.32, 95% CI: 1.03–1.68, P = 0.03)
DR and DNR or NPDR and DNR
A–3826G Chinese: hypertensive subjects M = 573 and F = 589; normotensive subjects M = 373 and F = 672 EH AA: 25.12%, AG: 50.85%, GG: 24.06%, G allele: 49.47% in normotensives;
AA: 25.22%, AG: 52.01%, GG: 22.77%, G allele: 48.78% in hypertensives
(Sun et al. 2018)
A–3826G Chinese: T2D patients N = 3107, including DR = 662 DR (OR = 1.001, P = 0.993) AA (n): 2578, AC (n): 469, CC (n): 14 (Jin et al. 2020)
A–1766G DR (OR = 0.949, P = 0.488)
A–112C + DR (OR = 1.368, P = 0.004)
A–1766G Chinese: T2D patients N = 929, nondiabetic controls N = 1044 + ↑ risk of T2D (OR = 1.42, P = 0.042), ↑ level of TG (β = 0.048, P = 0.034) under recessive model AA: 53.8%, AG: 37.3%, GG: 8.9%,
G allele: 27.6% in T2D patients;
AA: 53%, AG: 40.6%, GG: 6.4%,
G allele: 26.7% in controls
(Dong et al. 2020)
A–3826G Colombian: T2D cases M = 190 and F = 355; controls M = 126 and F = 323 + A allele and T2D (OR = 0.78; 95% CI: 0.63–0.97; P = 0.02) A allele: 0.54 in T2D cases and 0.60 in controls (Franco-Hincapié et al. 2014)
A–3826G Danes:young healthy subjects M = 177 and F = 176 BMI, fat mass, or weight gain during childhood and adolescence G allele: 25.3% (95% CI: 22.2–28.4%) (Urhammer et al. 1997)
Ala64Thr Danes: males with juvenile obesity N = 156; controls N = 205: lean controls N = 79 Obesity and weight gain during childhood or adolescence, or insulin sensitivity 64Thr allele: 8.2% in juvenile obese subjects, 8.8% in controls, and 8.2% in lean controls
Met229Leu 229Leu allele: 8.2% in obese subjects, 8.1% in controls, and 5.6% in lean controls
A–3826G Finnish: T2D patients M = 38 and F = 32; controls M = 55 and F = 68 T2D, body weight or BMI in diabetics or controls G allele: 38.6% in diabetics, 34.1% in controls (Sivenius et al. 2000)
A–3826G Finnish: obese premenopausal women N = 77 Weight gain after a VLCD G allele: 0.19 (Fogelholm et al. 1998)
A–3826G French: overweight patients N = 163 + ↓ weight loss after low calorie diet (P < 0.05) G allele: 0.27 (Fumeron et al. 1996)
A–3826G German: T2D patients N = 517 Neuropathy (P = 0.79), retinopathy
(P = 0.48), and nephropathy (P = 0.93)
AA: 49.9%, AG: 45.6%, GG: 4.5%,
G allele: 0.27
(Rudofsky et al. 2007)
Ala64Thr German children and adolescents: obese subjects N = 293, F = 53%; lean subjects N = 134, F = 46% Early-onset obesity 64Thr allele: 8.2% in obese, 4.1% in lean individuals (Hamann et al. 1998)
Met229Leu 229Leu allele: 10.4% in obese, 12.0% in lean individuals
A–3826G Indian: M = 49 and F = 47 + GG genotype and BMI (P < 0.01), SBP
(P < 0.01) and DBP (P < 0.05) in females
GG:13.5%, AG: 46.5%, AA: 39.9% (Dhall et al. 2012)
A–3826G Indian: T2D subjects M = 353 and F = 457; normal glucose-tolerant subjects M = 374 and F = 616 T2D AA: 36%, AG: 46%, GG: 18%
G allele: 0.41 in T2D subjects.
AA: 40%, AG: 45%, GG: 15%
G allele: 0.38 in normal glucose-tolerant subjects
(Vimaleswaran et al. 2009)
A–112C AA: 63%, AC: 33%, CC: 4%,
C allele: 0.21 in T2D subjects.
AA: 62%, AC: 34%, CC: 4%,
C allele: 0.21 in normal glucose- tolerant subjects
Met299Leu MetMet: 76%, MetLeu: 23%, LeuLeu: 1%, 299Leu allele: 0.12 in T2D subjects; MetMet: 73%, MetLeu: 26%, LeuLeu: 1%, 299Leu allele: 0.14 in normal glucose-tolerant subjects
A–3826G Italian: severely obese nondiabetic individuals M = 40 and F = 72 + IR in morbid obesity AA: 25.9%, AG + GG: 74.1% in total obese population;
AG + GG: 88% in IR (+) and
63% in IR (−) (OR = 4.3, 95% CI: 1.6–11.7; P = 0.003)
(Bracale et al. 2012)
A–3826G Italian: T2D individuals M = 56.6%; controls M = 41.2% T2D (OR = 0.85, 95% CI: 0.65–1.11; P = 0.221) G allele: 0.24 (Montesanto et al. 2018)
+ Risk of nephropathy (OR = 0.57, 95% CI: 0.33–0.98; P = 0.031)
Ischemic heart disease and stroke (OR = 1.10, 95% CI: 0.74–1.64; P = 0.643)
Ala64Thr T2D (OR = 0.99, 95% CI: 0.61–1.6;
P = 0.969)
64Thr allele: 0.063
+ Risk of retinopathy (OR = 0.31, 95% CI: 0.12–0.82; P = 0.010)
Ischemic heart disease and stroke (OR = 1.08, 95% CI: 0.52–2.26; P = 0.837)
A–3826G Japanese: individuals sampled during cold N = 1080 and hot season N = 979 + VFA during cold season (P = 0.0197) G allele: 0.51 (Nakayama et al. 2013)
A–3826G Japanese: subjects without a history of cardiovascular disease M = 231 and F = 347 + GG genotype and HT in males (OR = 2.32, 95% CI: 1.08–4.99) and older subjects (OR = 1.89, 95% CI: 1.00–3.57) AA: 24.0%, AG: 50.0%, GG: 26.0%,
G allele: 0.51
(Kotani et al. 2007)
A–112C Japanese: T2D patients M = 180 and F = 140, controls M = 145 and F = 105 + T2D (P = 0.017) С allele: 6.2% in healthy controls, 10.2% in T2D patients (Mori et al. 2001)
Met299Leu + T2D (P = 0.038) 229Leu allele: 7.2% in healthy controls, 10.8% in T2D patients
A–3826G T2D G allele: 53.6% in healthy controls, 49.7% in T2D patients
A–112C Japanese: T2D cases M = 55 and F = 38 + ↑ FIRI (P = 0.0085), HOMA-IR (P = 0.0089), and HLC (P = 0.012) AA: 88.2%, AC: 10.7%, CC:1.1% (Fukuyama et al. 2006)
A–3826G T2D AA: 32.3%, AG: 48.4%, GG: 19.3%
A–3826G Japanese: obese F = 113, healthy non-obese F = 76 + GG genotype and resistance to weight loss among obese (P < 0.05) G allele: 0.46 in obese and 0.45 in healthy non-obese (Kogure et al. 1998)
A–3826G Japanese: healthy
postmenopausal group F = 182 and premenopausal group F = 99
+ ↑ body weight (P = 0.048) in premenopausal women and changes in serum TG (P = 0.049) and HDL (P = 0.020) levels in postmenopausal women AA: 23.7%, AG: 53.2%, GG: 23.1%,
G allele: 0.50
(Matsushita et al. 2003)
A–3826G Japanese: healthy boys N = 22 + GG genotype and ↓ TEM to fat intake
(P < 0.05)
AA+AG (n): 13, GG (n): 9 (Nagai et al. 2003)
A–3826G Japanese: healthy children N = 19 + GG genotype and ↓ cold-induced thermogenesis (P < 0.05) AA+AG (n): 14, GG (n): 5 (Nagai et al. 2007)
A–3826G Japanese: M = 251 + AG genotype and BMI (P = 0.016) AA: 24.3%, AG: 48.2%, GG: 27.5% (Nakano et al. 2006)
A–3826G Korean: obese patients M = 44 and F = 146 + AG/GG genotypes and ↑ DBP (P = 0.023) and LDL-C (P = 0.011); GG genotype and ↓ HDL-C (P < 0.05) and ↑ atherogenic index AA: 22.1%, AG: 53.7%, GG: 24.2%,
G allele: 0.51
(Oh et al. 2004)
A–3826G Korean: F = 387 + [−3826G/−1766G] Ht and ↑ body fat percent (P = 0.045) NA (Kim et al. 2005)
A–1766G + AG/GG genotypes and abdominal subcutaneous fat (P = 0.015), abdominal visceral fat (P = 0.013), ↑ WHR (P = 0.008), body fat mass (P = 0.023), and percent body fat (P = 0.014) AA:57.4%, AG: 37.7%, GG: 4.9%, G allele: 0.238
A–3826G A–1766G
Ala64Thr
Korean: overweight F = 453 + [−3826G/ –1766A/64Thr] Ht and ↓ abdominal fat tissue area (P = 0.02), fat tissue area at thigh (P = 0.008), body fat mass (P = 0.002), and WHR (P = 0.01)
[−3826G/ –1766A/64Ala] Ht and reduction of WHR and body fat mass by VLCD
(P = 0.05–0.006)
NA (Shin et al. 2005)
A–3826G Mexican adolescents: normal weight N = 159 and overweight/obese N = 111 + ↑ percentage of fat (P = 0.002) and muscle weight (P = 0.019) in a recessive model AA: 16.2%, AG: 55.9%, GG: 27.9% in obese; AA: 17%, AG: 50.9%, GG: 32.1% in controls (Sámano et al. 2018)
A–3826G Mixed ethnicity population: obese patients N = 150, F = 80% + ↓ values of weight, body fat and free fat mass
(P < 0.05); GG genotype and ↓ tendency of T2D
AA: 41.3%, AG: 45.3%, GG: 13.4%,
G allele: 0.36
(Nicoletti et al. 2016)
A–3826G Polish: overweight/obese individuals M = 38 and F = 80 BMI AA: 51.38%, AG: 33.94%, GG:14.68%; G allele: 30.5%. (Kieć-Wilk et al. 2002)
+ ↑ fasting levels of TG (P < 0.04) and
↓ HDL-C (P = 0.004)
A–3826G Polish: embers of obese Caucasian families M = 38 and F = 84 Susceptibility to obesity and glucose tolerance parameters NA (Malczewska-Malec et al. 2004)
A–112C Saudi Arabian: obese patients M = 138 and F = 199; healthy volunteers M = 76 and F = 79 Obesity A allele/C allele (n/n): 627/47 in obese patients, 283/27 in controls (Chathoth et al. 2018)
A–1766G + A allele and moderate obesity (OR = 2.89, 95% CI 1.33–6.25; P = 0.007) A allele/G allele (n/n): 624/50 in obese patients, 298/12 in controls
A–3826G + Obesity after adjusting age, sex, and T2D (OR = 1.52, 95% CI: 1.10–2.08; P = 0.009) A allele/G allele (n/n): 443/231 in obese patients, 227/83 in controls
A–3826G Spanish: obese individuals N = 159, normal weight, N = 154 + ↑ BMI (P = 0.03), ↑ percentage of body fat
(P < 0.04), ↑ SBP (P = 0.009), ↑ DBP
(P = 0.02) in obese group
G allele: 0.21 in healthy, 0.19 in obese individuals (P = 0.574) (Forga et al. 2003)
A–3826G Spanish: obese M = 38 and F = 55; non-obese M = 122 and F = 117 + Obesity in women (P = 0.019) G allele: 0.3 in obese (0.28 in males and 0.31 in females), 0.24 in non-obese (0.32 in males and 0.17 in females) (P = 0.008) (Ramis et al. 2004)
A–3826G Swedish: obese subjects M = 310 and F = 364, non-obese subjects M = 54 and F = 257 Obesity-related phenotypes and weight gain G allele: 0.25 in obese, 0.24 in non-obese subjects (Gagnon et al. 1998)
A–3826G Turkish:obese M = 83 and F = 63; lean individuals M = 77 and F = 17 + ↑cholesterol levels G allele: 0.30 in obese, 0.31 in lean individuals (Proenza et al. 2000)
A–3826G Turkish children and adolescents: obese N = 268 and non-obese = 185 + GG denotype and obesity (OR = 2.02, 95% CI 1.17–3.47; P = 0.010),↑ TG levels in obese subjects (P = 0.048), ↓ HDL-C (P = 0.017) AA: 46.3%, AG: 33.2%, GG: 20.5%,
G allele: 37.1% in obese;
AA: 46.5%, AG: 42.2%, GG: 11.4%,
G allele: 32.4% in controls
(Gul et al. 2017)
Ala64Thr White subjects: obese N = 93 and non-obese N = 69 BMI or obesity 64Thr allele: 12.0% (Herrmann et al. 2003)
+ WHR (P = 0.003) after adjustment for gender, age, BMI, and T2D
  1. Abbreviations: F Females, M Males, BMI Body mass index, RMR Resting metabolic rate, DR Diabetic retinopathy, PDR Prolifirative diabetic retinopathy, NPDR Non-prolifirative diabetic retinopathy, DNR Diabetes without retinopathy, EH Essential hypertension, T2D Type 2 diabetes, VLCD Very low calorie diet, IR Insulin resistance, VFA Visceral fat accumulation, HT Hypertension, FIRI Fasting insulin resistance index, HOMA-IR Homoeostasis model assessment of insulin resistance, HLC Hepatic lipid content, HDL-C High density lipoprotein cholesterol, TEM Thermic effect of a meal, Ht Haplotype, SBP Systolic blood pressure, DPB Diastolic blood pressure, LDL-C Low density lipoprotein cholesterol, WHR Waist-to-hip ratio, TG Trygliceride, NA Not available