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 | ||||