AGPAT3 deficiency impairs adipocyte differentiation and leads to a lean phenotype in mice.

Acylglycerophosphate acyltransferases (AGPATs) catalyze the de novo formation of phosphatidic acid to synthesize glycerophospholipids and triglycerides. AGPATs demonstrate unique physiological roles despite a similar biochemical function. AGPAT3 is highly expressed in the testis, kidney, and liver, with intermediate expression in adipose tissue. Loss of AGPAT3 is associated with reproductive abnormalities and visual dysfunction. However, the role of AGPAT3 in adipose tissue and whole body metabolism has not been investigated. We found that male Agpat3 knockout (KO) mice exhibited reduced body weights with decreased white and brown adipose tissue mass. Such changes were less pronounced in the female Agpat3-KO mice. Agpat3-KO mice have reduced plasma insulin growth factor 1 (IGF1) and insulin levels and diminished circulating lipid metabolites. They manifested intact glucose homeostasis and insulin sensitivity despite a lean phenotype. Agpat3-KO mice maintained an energy balance with normal food intake, energy expenditure, and physical activity, except for increased water intake. Their adaptive thermogenesis was also normal despite reduced brown adipose mass and triglyceride content. Mechanistically, Agpat3 was elevated during mouse and human adipogenesis and enriched in adipocytes. Agpat3-knockdown 3T3-L1 cells and Agpat3-deficient mouse embryonic fibroblasts (MEFs) have impaired adipogenesis in vitro. Interestingly, pioglitazone treatment rescued the adipogenic deficiency in Agpat3-deficient cells. We conclude that AGPAT3 regulates adipogenesis and adipose development. It is possible that adipogenic impairment in Agpat3-deficient cells potentially leads to reduced adipose mass. Findings from this work support the unique role of AGPAT3 in adipose tissue.NEW & NOTEWORTHY AGPAT3 deficiency results in male-specific growth retardation. It reduces adipose tissue mass but does not significantly impact glucose homeostasis or energy balance, except for influencing water intake in mice. Like AGPAT2, AGPAT3 is upregulated during adipogenesis, potentially by peroxisome proliferator-activated receptor gamma (PPARγ). Loss of AGPAT3 impairs adipocyte differentiation, which could be rescued by pioglitazone. Overall, AGPAT3 plays a significant role in regulating adipose tissue mass, partially involving its influence on adipocyte differentiation.

Early Operation for Complications Arising From Bariatric Surgical Tourism.

The patient is a 48-year-old female, who underwent LAGB in Tijuana, Mexico, via bariatric medical tourism in 2008. She had no follow up after surgery. Subsequently had a port infection, for which the port was removed, but the band was left in place. Suffered with chronic abdominal pain for many years before the retained band was recognized. During band removal, it was discovered that she had complete band erosion. After removal, her symptoms resolved. This case demonstrates the issues with bariatric medical tourism. Specifically, because of the lack of appropriate follow up. Follow up and monitoring after surgery is important for preventing bariatric surgery complications and assisting with adequate weight loss. The other aspect of the case is the importance to recognize bariatric surgery complications. Port infection should warrant an investigation for potential intra-abdominal sources. Band erosion is uncommon but known complication of LAGB and requires band removal.

Pneumoperitoneum and PEG Dislodgement Secondary to Noninvasive Ventilation after PEG Tube Placement.

We present a previously undescribed complication after noninvasive ventilation (NIV) for respiratory failure in a patient who required percutaneous endoscopic gastrostomy (PEG) tube placement for long-term nutrition after a complicated coronary bypass operation. A 54-year-old female diagnosed with unilateral vocal cord paralysis after emergent coronary artery bypass grafting (CABG) underwent an uncomplicated PEG tube placement. She was placed on intermittent NIV because of respiratory failure 24 hours after PEG placement, and NIV was continued for several days. Three days later, she was noted to have pneumoperitoneum on an upright chest X-ray. Abdominal CT scan revealed a large amount of pneumoperitoneum with the PEG tube in the correct position and no extravasation of enteric contrast from the stomach. Tube feeds were held and NIV was discontinued. Nonetheless, six days later, the patient was found on CT scan to have partial displacement of the PEG tube with leakage from the gastrotomy requiring operative repair. This case highlights the vulnerability of PEG tubes to management practices in the early postoperative period. Abdominal distention secondary to NIV likely caused pressure necrosis of the PEG site with dislodgement of the tube. This case elicits considerations regarding future management practices of patients receiving NIV in the early postoperative period after PEG placement.