To evaluate mitochondrial respiratory capacity, mitochondrial content, and UCP1 gene expression in white adipose tissue from women with obesity before and after the physical training program.
These results reveal a role for Egr1 in blocking energy expenditure via direct Ucp1 transcription repression and highlight Egr1 as a therapeutic target for counteracting obesity.
Human UCP3 is different from UCP1 and UCP2 by its high and preferential expression in skeletal muscle and consequently the UCP3 gene is an attractive candidate gene for obesity.
The absence of UCP1 augmented obesity (weight gain, body fat mass, %body fat, fat depot size) in high-fat diet- and cafeteria-fed mice, with a similar or lower food intake, indicating that, when present, UCP1 indeed decreases metabolic efficiency.
Intake of a high-fat diet rich in omega-3 fatty acids protects both wild-type and UCP1-deficient mice from obesity and insulin resistance by increasing energy expenditure through unknown mechanisms.
We now report the discovery of a gene that codes for a novel uncoupling protein, designated UCP2, which has 59% amino-acid identity to UCP1, and describe properties consistent with a role in diabetes and obesity.
Our study aimed to examine the mechanisms through which obesity induced by a high fat diet (HFD) affects uncoupling protein 1 (UCP1) expression via signal transduction and activator of transcription 5 (STAT5s).
Ucp1 induction by stimuli including cold, exercise, and diet increases nonshivering thermogenesis, leading to increased energy expenditure and prevention of obesity.
In three experiments of similar setup, uncoupling protein 1-ablated mice fed a high‑fat diet had either reduced or similar body mass gain, food intake and metabolic efficiency compared to wildtype mice, challenging the hypothesized role of this protein in the development of diet-induced obesity.
To study associations of UCP gene expression with human obesity, we determined, by a competitive reverse transcription-polymerase chain reaction assay, UCP mRNA expression levels in intra- and extraperitoneal adipose tissues of 79 obese subjects and 17 lean controls.
In addition to sympathetic nerve-derived NE, the intestinal microbiota was involved in the increase in NE.Infection with <i>H. polygyrus</i> altered the composition of intestinal bacteria, and antibiotic treatment to reduce intestinal bacteria reversed the higher NE concentration, UCP1 expression, and prevention of the weight gain observed after <i>H. polygyrus</i> infection.Our data indicate that <i>H. polygyrus</i> exerts suppressive roles on obesity through modulation of microbiota that produce NE.
The HFF diet promoted obesity.Treatment with Vm24 did not alter various metabolic parameters such as food intake, BW gain, visceral white adipose tissue mass, adipocyte diameter, serum glucose, leptin and thyroid hormone concentrations, brown adipose tissue mass or uncoupling protein-1 expression, and insulin tolerance.
Our results clearly showed that <i>UCP1</i>-VAT expression was significantly increased in severe human obesity (BMI > 50 kg/m<sup>2</sup>) and that it behaved as an independent predictor of REE.
In our case-control study we were not able to demonstrate any association between UCP polymorphisms and obesity in T2DM patients; however, in the meta-analysis we detected a significant association of UCP2 -866G/A, Ins/Del, Ala55Val and UCP3 -55C/T polymorphisms with obesity.
Studies in a Ucp-1 reporter mouse model revealed that early intervention with ARA/DHA and eHC improves metabolic flexibility and attenuates obesity during HFD challenge later in life.