Efficacy of low-level laser therapy for body contouring and spot fat reduction.

BACKGROUND: Low-level laser therapy (LLLT) is commonly used in medical applications, but scientific studies of its efficacy and the mechanism by which it causes loss of fat from fat cells for body contouring are lacking. This study examined the effectiveness and mechanism by which 635­680 nm LLLT acts as a non-invasive body contouring intervention method. METHODS: Forty healthy men and women ages 18­65 years with a BMI <30 kg/m2 were randomized 1:1 to laser or control treatment. Subject's waistlines were treated 30 min twice a week for 4 weeks. Standardized waist circumference measurements and photographs were taken before and after treatments 1, 3, and 8. Subjects were asked not to change their diet or exercise habits. In vitro assays were conducted to determine cell lysis, glycerol, and triglyceride release. RESULTS: Data were analyzed for those with body weight fluctuations within 1.5 kg during 4 weeks of the study. Each treatment gave a 0.4­0.5 cm loss in waist girth.Cumulative girth loss after 4 weeks was −2.15 cm (−0.78 ± 2.82 vs. 1.35 ± 2.64 cm for the control group,p < 0.05). A blinded evaluation of standardized pictures showed statistically significant cosmetic improvement after 4 weeks of laser treatment. In vitro studies suggested that laser treatment increases fat loss from adipocytes by release of triglycerides, without inducing lipolysis or cell lysis. CONCLUSIONS: LLLT achieved safe and significant girth loss sustained over repeated treatments and cumulative over 4 weeks of eight treatments. The girth loss from the waist gave clinically and statistically significant cosmetic improvement.

The ubiquitin carboxyl hydrolase BAP1 forms a ternary complex with YY1 and HCF-1 and is a critical regulator of gene expression.

The candidate tumor suppressor BAP1 is a deubiquitinating enzyme (DUB) involved in the regulation of cell proliferation, although the molecular mechanisms governing its function remain poorly defined. BAP1 was recently shown to interact with and deubiquitinate the transcriptional regulator host cell factor 1 (HCF-1). Here we show that BAP1 assembles multiprotein complexes containing numerous transcription factors and cofactors, including HCF-1 and the transcription factor Yin Yang 1 (YY1). Through its coiled-coil motif, BAP1 directly interacts with the zinc fingers of YY1. Moreover, HCF-1 interacts with the middle region of YY1 encompassing the glycine-lysine-rich domain and is essential for the formation of a ternary complex with YY1 and BAP1 in vivo. BAP1 activates transcription in an enzymatic-activity-dependent manner and regulates the expression of a variety of genes involved in numerous cellular processes. We further show that BAP1 and HCF-1 are recruited by YY1 to the promoter of the cox7c gene, which encodes a mitochondrial protein used here as a model of BAP1-activated gene expression. Our findings (i) establish a direct link between BAP1 and the transcriptional control of genes regulating cell growth and proliferation and (ii) shed light on a novel mechanism of transcription regulation involving ubiquitin signaling.