Immunodetection of UCP1 in rat thymocytes

Carroll, A.M.; Haines, Lee R.; Pearson, Terry W.; Brennan, Clare M.; Breen, Edmond J.; Porter, Richard K.

doi:10.1042/bst0321066

Cited by 22 publications

(18 citation statements)

References 11 publications

(14 reference statements)

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“…UCP1 has been shown to be almost exclusively expressed in the brown fat conferring to this tissue its specific function in non-shivering thermogenesis [37], [45]. Although controversial, there is growing evidence that UCP1 is expressed in other tissues such as the thymus [46], the white adipose tissue and skeletal muscles [21], [23], [47], [48]. Mice devoid of RIP140 have increased oxygen consumption and respiratory exchange ratio compared to WT littermates [25] suggesting they utilize fatty acids as the main source of energy.…”

Section: Discussionmentioning

confidence: 99%

Absence of RIP140 Reveals a Pathway Regulating glut4-Dependent Glucose Uptake in Oxidative Skeletal Muscle through UCP1-Mediated Activation of AMPK

et al. 2012

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Skeletal muscle constitutes the major site of glucose uptake leading to increased removal of glucose from the circulation in response to insulin. Type 2 diabetes and obesity are often associated with insulin resistance that can be counteracted by exercise or the use of drugs increasing the relative proportion of oxidative fibers. RIP140 is a transcriptional coregulator with a central role in metabolic tissues and we tested the effect of modulating its level of expression on muscle glucose and lipid metabolism in two mice models. Here, we show that although RIP140 protein is expressed at the same level in both oxidative and glycolytic muscles, it inhibits both fatty acid and glucose utilization in a fiber-type dependent manner. In RIP140-null mice, fatty acid utilization increases in the extensor digitorum longus and this is associated with elevated expression of genes implicated in fatty acid binding and transport. In the RIP140-null soleus, depletion of RIP140 leads to increased GLUT4 trafficking and glucose uptake with no change in Akt activity. AMPK phosphorylation/activity is inhibited in the soleus of RIP140 transgenic mice and increased in RIP140-null soleus. This is associated with increased UCP1 expression and mitochondrial uncoupling revealing the existence of a signaling pathway controlling insulin-independent glucose uptake in the soleus of RIP140-null mice. In conclusion, our findings reinforce the participation of RIP140 in the maintenance of energy homeostasis by acting as an inhibitor of energy production and particularly point to RIP140 as a promising therapeutic target in the treatment of insulin resistance.

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Section: Discussionmentioning

confidence: 99%

Absence of RIP140 Reveals a Pathway Regulating glut4-Dependent Glucose Uptake in Oxidative Skeletal Muscle through UCP1-Mediated Activation of AMPK

et al. 2012

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“…However, expression of ucp1 in mouse brain, skeletal muscle [39] and uterus [40], and rat thymus [41] have been reported. The rapid insulin response measured by AIR g is generally believed to be a measure of beta cell function, and we therefore sought to explain the biological impact of UCP1 on AIR g by investigating the expression of this gene in the pancreas.…”

Section: Discussionmentioning

confidence: 99%

The uncoupling protein 1 gene, UCP1, is expressed in mammalian islet cells and associated with acute insulin response to glucose in African American families from the IRAS Family Study

et al. 2007

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BackgroundVariants of uncoupling protein genes UCP1 and UCP2 have been associated with a range of traits. We wished to evaluate contributions of known UCP1 and UCP2 variants to metabolic traits in the Insulin Resistance and Atherosclerosis (IRAS) Family Study.MethodsWe genotyped five promoter or coding single nucleotide polymorphisms (SNPs) in 239 African American (AA) participants and 583 Hispanic participants from San Antonio (SA) and San Luis Valley. Generalized estimating equations using a sandwich estimator of the variance and exchangeable correlation to account for familial correlation were computed for the test of genotypic association, and dominant, additive and recessive models. Tests were adjusted for age, gender and BMI (glucose homeostasis and lipid traits), or age and gender (obesity traits), and empirical P-values estimated using a gene dropping approach.ResultsUCP1 A-3826G was associated with AIRg in AA (P = 0.006) and approached significance in Hispanic families (P = 0.054); and with HDL-C levels in SA families (P = 0.0004). Although UCP1 expression is reported to be restricted to adipose tissue, RT-PCR indicated that UCP1 is expressed in human pancreas and MIN-6 cells, and immunohistochemistry demonstrated co-localization of UCP1 protein with insulin in human islets. UCP2 A55V was associated with waist circumference (P = 0.045) in AA, and BMI in SA (P = 0.018); and UCP2 G-866A with waist-to-hip ratio in AA (P = 0.016).ConclusionThis study suggests a functional variant of UCP1 contributes to the variance of AIRg in an AA population; the plausibility of this unexpected association is supported by the novel finding that UCP1 is expressed in islets.

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“…This important work highlights the power of comparative approaches to filter the data for functional elements and to distinguish between specific and general regulation of UCP1 in BAT. Although mammalian UCP1 expression appears specific for brown and beige adipose tissue, there are some reports of UCP1 expression in the thymus of mice and rats; however, the physiological role is not clarified yet (Adams et al, 2008a,b;Carroll et al, 2004;Carroll et al, 2005). Other claims are less convincing, such as the detection of UCP1 in murine smooth muscle cells, which has been disproven by others (Rousset et al, 2003).…”

Section: Evolution Of Ucp1 and Batmentioning

confidence: 99%

Insights into brown adipose tissue evolution and function from non-model organisms

Jastroch

Oelkrug

Keipert

2018

Journal of Experimental Biology

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Brown adipose tissue (BAT) enables adaptive thermoregulation through heat production that is catalyzed by mitochondrial uncoupling protein 1 (UCP1). BAT is frequently studied in rodent model organisms, and recently in adult humans to treat metabolic diseases. However, complementary studies of many non-model species, which have diversified to many more ecological niches, may significantly broaden our understanding of BAT regulation and its physiological roles. This Review highlights the research on non-model organisms, which was instrumental to the discovery of BAT function, and the unique evolutionary history of BAT/UCP1 in mammalian thermogenesis. The comparative biology of BAT provides a powerful integrative approach that could identify conserved and specialized functional changes in BAT and UCP1 by considering species diversity, ecology and evolution, and by fusing multiple scientific disciplines such as physiology and biochemistry. Thus, resolving the complete picture of BAT biology may fail if comparative studies of non-model organisms are neglected.

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Immunodetection of UCP1 in rat thymocytes

Cited by 22 publications

References 11 publications

Absence of RIP140 Reveals a Pathway Regulating glut4-Dependent Glucose Uptake in Oxidative Skeletal Muscle through UCP1-Mediated Activation of AMPK

Absence of RIP140 Reveals a Pathway Regulating glut4-Dependent Glucose Uptake in Oxidative Skeletal Muscle through UCP1-Mediated Activation of AMPK

The uncoupling protein 1 gene, UCP1, is expressed in mammalian islet cells and associated with acute insulin response to glucose in African American families from the IRAS Family Study

Insights into brown adipose tissue evolution and function from non-model organisms

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