Our aims were to evaluate the outcomes of TKR surgery and the risks for post-operative complications in patients with morbid obesity (BMI > 40 kg/m<sup>2</sup>) as compared with obese patients (30 < BMI ≤ 40 kg/m<sup>2</sup>) and non-obese patients, BMI < 30 kg/m<sup>2</sup>); to evaluate if there are differences between morbid-obese patients (BMI 40-49.99 kg/m<sup>2</sup>) and extreme morbid obese patients (BMI > 50 kg/m<sup>2</sup>); and to present some surgical tips which can improve the TKR outcomes in morbid obese patients.
Here, we further investigate the effects of MGAT2 inhibition on 1) fat-induced gut peptide release and fat intake in normal mice and 2) metabolic disorders in high-fat diet (HFD)-fed ob/ob mice, a model of severe obesity and type 2 diabetes mellitus, using an orally bioavailable MGAT2 inhibitor Compound B (CpdB).
Impact of morbid obesity (BMI > 40 kg/m<sup>2</sup>) on complication rate and outcome following minimally invasive transforaminal lumbar interbody fusion (MIS TLIF).
After CR, notwithstanding a greater percent weight reduction in obesity (-3.5% ± 6.9% vs +1.1% ± 7.0%, P = 0.002) and severe obesity (-6.5% ± 6.9% vs +1.1% ± 7.0%, P < 0.001), smaller improvements in PCS scores were seen in the obese (4.1 ± 7.4 vs 6.9 ± 7.6, P = 0.011) and severely obese (4.1 ± 7.6 vs 6.9 ± 7.6, P = 0.039) when compared with those with normal BMI.
This study determined the content of lipids (ceramide [CER], diacylglycerol [DAG], triacylglycerol, and free fatty acid [FFA]) and the expression of fatty acid translocase (FAT/CD36) and plasma membrane fatty acid-binding protein in visceral adipose tissue (VAT) and subcutaneous adipose tissue of women with morbid obesity without metabolic syndrome (MetSx-) or with metabolic syndrome (MetSx+) and compared the results with those of lean controls without metabolic syndrome.
To study the change in brown and white adipose tissue (BAT and WAT), as well as fat content in the liver and pancreas, in patients with morbid obesity before and after bariatric surgery.
Serum FGF21 was positively and significantly correlated to the expression of UCP1 (<i>r</i> = 0.56, <i>p</i> = 0.02) and TBX1 (<i>r</i> = 0.62, <i>p</i> = 0.01), however, this correlation was missing in patients with severe obesity.
Using model 2, an association was identified between an advanced disease stage and 2 factors: morbid obesity (OR, 1.9; P = .02) and positive human epidermal growth factor receptor 2 (OR, 1.8; P = .045).
However, the association between morbid obesity and AChE and the changes in cholinergic tone following bariatric laparoscopic sleeve gastrectomy (LSG) surgery-induced weight reduction were never analyzed.
The PE of (1) AktII and basal phosphorylated AktII (pAktII) showed no difference within the groups, (2) the 37 kDa and 34 kDa isoforms of AQP7 were decreased in Visc/Sub from OB/MOW/MODM, (3) GLUT4 was decreased in Visc/Sub from OB/MOW/MODM, and (4) the 34 kDa isoform of AQP7 was decreased in Sub of MODM compared with MOW.
We present a patient with morbid obesity who carries a known pathogenic PTEN mutation, identified at the bariatric surgery clinic using an obesity gene panel consisting of 52 obesity-associated genes.
The present study provides detailed progranulin gene expression data in sc and vis AT in a large, prospective and observational cohort of patients with severe obesity.
This is the first time that a heterozygous LMF1 nonsense variant was found in a HTG-AP patient with severe obesity and heavy smoking, highlighting an important interplay between genetic and lifestyle factors in the etiology of HTG.