The polymorphisms of UCP1 genes associated with fat metabolism, obesity and diabetes

Jia, Junjing; Tian, Yunbo; Cao, Zhenhui; Tao, Linli; Zhang, Xi; Gao, Shumin; Ge, Chao; Lin, Qiu-Ye; Jois, Markandeya

doi:10.1007/s11033-009-9550-2

Cited by 89 publications

(62 citation statements)

References 83 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The principle function of BAT is to regulate energy expenditure via non-shivering thermogenesis; UCP-1, a mitochondrial membrane protein, plays a key role [23]. UCP-1 expression in BAT is closely linked to obesity and diabetes [33]. Genetic ablation of BAT results in the development of obesity without hyperphagia in animal models [34].…”

Section: Discussionmentioning

confidence: 99%

Anti-Obesity Effects of Granulocyte-Colony Stimulating Factor in Otsuka-Long-Evans-Tokushima Fatty Rats

et al. 2014

View full text Add to dashboard Cite

Granulocyte-colony stimulating factor (G-CSF) has molecular structures and intracellular signaling pathways that are similar to those of leptin and ciliary neurotropic factor (CNTF). It also has immune-modulatory properties. Given that leptin and CNTF play important roles in energy homeostasis and that obesity is an inflammatory condition in adipose tissue, we hypothesized that G-CSF could also play a role in energy homeostasis. We treated 12 38-week-old male Otsuka-Long-Evans-Tokushima fatty rats (OLETF, diabetic) and 12 age-matched male Long-Evans-Tokushima rats (LETO, healthy) with 200 µg/day G-CSF or saline for 5 consecutive days. Body weight reduction was greater in G-CSF-treated OLETF (G-CSF/OLETF) than saline-treated OLETF (saline/OLETF) following 8 weeks of treatment (−6.9±1.6% vs. −3.1±2.2%, p<0.05). G-CSF treatment had no effect on body weight in LETO or on food intake in either OLETF or LETO. Body fat in G-CSF/OLETF was more reduced than in saline/OLETF (−32.2±3.1% vs. −20.8±6.2%, p<0.05). Energy expenditure was higher in G-CSF/OLETF from 4 weeks after the treatments than in saline/OLETF. Serum levels of cholesterol, triglyceride, interleukin-6 and tumor necrosis factor-α were lower in G-CSF/OLETF than in saline/OLETF. Uncoupling protein-1 (UCP-1) expression in brown adipose tissue (BAT) was higher in G-CSF/OLETF than in saline/OLETF, but was unaffected in LETO. Immunofluorescence staining and PCR results revealed that G-CSF receptors were expressed in BAT. In vitro experiments using brown adipocyte primary culture revealed that G-CSF enhanced UCP-1 expression from mature brown adipocytes via p38 mitogen-activated protein kinase pathway. In conclusion, G-CSF treatment reduced body weight and increased energy expenditure in a diabetic model, and enhanced UCP-1 expression and decreased inflammatory cytokine levels may be associated with the effects of G-CSF treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

Anti-Obesity Effects of Granulocyte-Colony Stimulating Factor in Otsuka-Long-Evans-Tokushima Fatty Rats

et al. 2014

View full text Add to dashboard Cite

show abstract

“…7 The thermogenic activity of BAT depends on its quantity, its UCP1 content, and the extent of stimulation of the sympathetic nervous system (SNS). 7 Accordingly, genetic polymorphism, such as the -3826 A/G single nucleotide polymorphism in the promoter in exon 2 of UCP1, has been reported to be associated with obesity phenotypes 8 causing reduced mRNA expression. 9 We previously reported that healthy children with the G/G genotype had a lower capacity for thermogenesis in response to a high-fat meal 10 and acute cold exposure.…”

Section: Introductionmentioning

confidence: 99%

UCP1 genetic polymorphism (–3826 A/G) diminishes resting energy expenditure and thermoregulatory sympathetic nervous system activity in young females

et al. 2010

View full text Add to dashboard Cite

Background: Recent findings regarding the existence of functional brown adipose tissue (BAT) in adult humans suggest a physiological role of BAT and uncoupling protein 1 (UCP1)-linked thermogenesis in energy balance. Objective: To investigate whether UCP1 polymorphism was associated with resting energy expenditure (REE) and thermoregulatory sympathetic nervous system (SNS) activity in humans. Methods: A total of 82 healthy females (20-22 years) were genotyped for the -3826 A/G polymorphism of the UCP1 gene using a fluorescent allele-specific DNA primer assay system. REE was measured by indirect calorimetry. The thermoregulatory SNS activity was assessed by heart rate variability power spectral analysis according to our previously reported method. Each subject was studied in the morning, after an overnight fast. Nutritional values were calculated on the basis of 2-day food records.

show abstract

“…Though less defined at this stage there is also growing evidence that other innate biological differences may occur that make some people more susceptible than others to obesity. These include differences in hypothalamic-pituitary axis (HPA) axis function [18] or in basal energy expenditure for example as a result of mitochondrial function [19] or uncoupling proteins and non-shivering thermogenesis [20][21][22].…”

Section: Physiological Aspects Of Obesity: Energy Homeostasismentioning

confidence: 99%

Women, Biology, Obesity and Health: Implications of the Emerging Bioscience Research

Penny¹,

Page²

2013

Bioenergetics

View full text Add to dashboard Cite

IntroductionHelen at 59 years of age with a height of 170 cm and a weight of 136 kg has a BMI of 49 kg/m 2 which classifies her as being seriously obese. She is a health professional and well aware of the health risks associated with her excess weight. She is also a woman living in a society where a slim body is perceived as an essential requirement for feminine beauty and fashion. Over the years Helen has tried most non-fat diets as well as various drugs in her attempts to lose weight. Instead there has been a relentless increase in weight from 82 kg after the birth of her two children when she was 21 years old (a BMI of 28.5 kg/m 2 ) to her current weight and BMI which persists in spite of her healthy diet and not excessive kilojoules intake [1]. Helen is not alone; there are many other women who can testify to similar long term battles against excess weight gain [2,3]. Too often for some, attempts to lose weight leads to frustration, guilt and ultimately failure and a pre-occupation with food and dieting that may for some lead on to eating disorders. Women are not only more vulnerable to these psychological pressures [4], but also their intrinsic physiological make up makes them more prone to weight gain.Cheap energy dense food in generous portions that is too easily accessible and a sedentary life style in conjunction with socioeconomic factors such as food insecurity and lack of nutritional understanding are certainly important contributing factors to weight gain. But the question remains why, in any community, there are some who find it easier to remain slim, in spite of sharing the same obesogenic environment while others like Helen, a health conscious well informed professional, become increasingly obese. An accumulating body of emerging research in neuroscience and molecular biosciences confirms what many women know well from personal experience -that slimness is not simply a matter of willpower and diet and easily obtainable by all. The objective of this paper is to provide a broad-based literature search on current research in genetics, early development, environmental factors, gender and physiological pathways that regulate energy turnover and discuss how these may affect body fat storage in the body and biological vulnerability to obesity. Physiological Aspects of Obesity: Energy HomeostasisEnergy homeostasis involves complex sophisticated neurohormonal pathways that regulate energy balance and ensure adequate energy stores to meet increased demands for growth in children and it is particularly significant for women during pregnancy and lactation. This can be seen in the rapid increase in fat deposition that occurs particularly in critical periods during the human life span: prior to and during pregnancy and in the baby, prior to birth, during the first 6 months of life and prior to weaning [5]. The existence of these energy regulating mechanisms is also seen in the remarkable constancy of human weight, often over many years (and without calorie counting!) for some, and in the resistance to weight c...

show abstract

The polymorphisms of UCP1 genes associated with fat metabolism, obesity and diabetes

Cited by 89 publications

References 83 publications

Anti-Obesity Effects of Granulocyte-Colony Stimulating Factor in Otsuka-Long-Evans-Tokushima Fatty Rats

Anti-Obesity Effects of Granulocyte-Colony Stimulating Factor in Otsuka-Long-Evans-Tokushima Fatty Rats

UCP1 genetic polymorphism (–3826 A/G) diminishes resting energy expenditure and thermoregulatory sympathetic nervous system activity in young females

Women, Biology, Obesity and Health: Implications of the Emerging Bioscience Research

Contact Info

Product

Resources

About