Alessandro Scarda

Sleeve gastrectomy as revisional procedure for failed gastric banding or gastroplasty

BACKGROUND Laparoscopic sleeve gastrectomy (LSG) is considered an effective multipurpose operation for morbid obesity, although long-term results are still lacking. Also, the best procedure to be offered in the case of failed restrictive procedures is still debated. We here reported our results of LSG as a revisional procedure for inadequate weight loss and/or complications after adjustable gastric banding or gastroplasty. METHODS Since April 2005, 57 patients (20 men and 37 women), with a mean age of 49.9 +/- 11.9 years, underwent revisional LSG, 52 after laparoscopic adjustable gastric banding/adjustable gastric banding and 5 after vertical banded gastroplasty at our institution. The mean interval from the primary procedure to LSG was 7.54 +/- 4.8 years. The LSG was created using a 34F bougie with an endostapler, after removing the laparoscopic adjustable gastric band or the anterior portion of the band in those who had undergone vertical banded gastroplasty. An upper gastrointestinal contrast study was performed within 3 days after surgery and, if the findings were negative, a soft diet was promptly started. RESULTS A total of 41 patients had undergone concurrent band removal and LSG and 16 had undergone band removal followed by an interval LSG. Three cases required conversion to open surgery because of a large incisional hernia. The mean operative time was 120 minutes (range 90-180). One patient died of multiple organ failure from septic shock. Three patients (5.7%) developed a perigastric hematoma, 3 (5.7%) had leaks, and 1 had mid-gastric short stenosis. The median hospital stay was 5 days. The mean body mass index at revisional LSG was 45.7 +/- 10.8 kg/m(2) and had decreased to 39 +/- 8.5 kg/m(2) after 2 years, with a mean percentage of the estimated excess body mass index lost of 41.6% +/- 24.4%. Two patients required a duodenal switch for insufficient weight loss. CONCLUSION LSG seems to be effective as revisional procedure for failed LAGB/vertical banded gastroplasty, although with greater complication rates than the primary procedures. Larger series and longer follow-up are needed to confirm these promising results.

Rosiglitazone modifies the adipogenic potential of human muscle satellite cells.

Aims/hypothesisSatellite cells are responsible for postnatal skeletal muscle regeneration. It has been demonstrated that mouse satellite cells behave as multipotent stem cells. We studied the differentiation capacities of human satellite cells and evaluated the effect of the insulin sensitiser rosiglitazone, a well known peroxisome proliferative activated receptor gamma (PPARG) agonist, on their adipogenic conversion.Subjects, materials and methodsWe obtained human satellite cells from human muscle biopsies of healthy subjects by single-fibre isolation and cultured them under myogenic, osteogenic and adipogenic conditions. Moreover, we compared the morphological features and the adipose-specific gene expression profiling, as assessed by quantitative PCR, between adipocytes differentiated from human satellite cells and those obtained from the stromal vascular fraction of human visceral fat.ResultsWe proved by morphological analysis, mRNA expression and immunohistochemistry that human satellite cells are able to differentiate into myotubes, adipocytes and osteocytes. The addition of rosiglitazone to the adipogenic medium strongly activated PPARG expression and enhanced adipogenesis in human satellite cells, but did not in itself trigger the complete adipogenic programme. Moreover, we observed a decrease in wingless-type MMTV integration site family member 10B and an upregulation of growth differentiation factor 8 expression, both being independent of PPARG activation.Conclusions/interpretationHuman satellite cells possess a clear adipogenic potential that could explain the presence of mature adipocytes within skeletal muscle in pathological conditions such as obesity, type 2 diabetes and ageing-related sarcopenia. Rosiglitazone treatment, while enhancing adipogenesis, induces a more favourable pattern of adipocytokine expression in satellite-derived fat cells. This could partially counteract the worsening effect of intermuscular adipose tissue depots on muscle insulin sensitivity.

Increased adipogenic conversion of muscle satellite cells in obese Zucker rats

Aims/hypothesis:Visceral and intermuscular adipose tissue (IMAT) depots account for most obesity-related metabolic and cardiovascular complications. Muscle satellite cells (SCs) are mesenchymal stem cells giving rise to myotubes and also to adipocytes, suggesting their possible contribution to IMAT origin and expansion. We investigated the myogenic differentiation of SCs and the adipogenic potential of both preadipocytes and SCs from genetically obese Zucker rats (fa/fa), focusing on the role of Wnt signaling in these differentiation processes.Methods:SCs were isolated by single-fiber technique from flexor digitorum brevis muscle and preadipocytes were extracted from subcutaneous adipose tissue (AT). Morphological features and gene expression profile were evaluated during in vitro myogenesis and adipogenesis. Wingless-type MMTV integration site family member 10b (Wnt10b) expression was quantified by quantitative PCR in skeletal muscle and AT.Results:We did not observe any difference in the proliferation rate and in the myogenic differentiation of SCs from obese and lean rats. However, a decreased insulin-induced glucose uptake was present in myotubes originating from fa/fa rats. Under adipogenic conditions, preadipocytes and SCs of obese animals displayed an enhanced adipogenesis. Wnt10b expression was reduced in obese rats in both muscle and AT.Conclusions/interpretation:Our data suggest that the increase in different fat depots including IMAT and the reduced muscle insulin sensitivity, the major phenotypical alteration of obese Zucker rats, could be ascribed to an intrinsic defect, either genetically determined or acquired, still present in both muscle and fat precursors. The involvement of Wnt10b as a regulator of both adipogenesis and muscle-to-fat conversion is suggested.

Androgens modulate osteocalcin release by human visceral adipose tissue.

Objective  Androgens inhibit adipogenic differentiation through an androgen receptor (AR)‐mediated pathway, increase lipolysis and reduce lipid accumulation in adipocytes. Undercarboxylated osteocalcin (ucOCN) regulates insulin and adiponectin secretion and is released by adipose tissue (AT). Our objective was to investigate, ex vivo and in vivo, the role of androgens on osteocalcin (OCN) modulation in human AT.

Presence of anti-ADAMTS13 antibodies in obesity

Eur J Clin Invest 2012; 42 (11): 1197–1204

Adipogenic potential of skeletal muscle satellite cells

Abstract Satellite cells (SCs) are undifferentiated skeletal muscle cells that allow muscular growth and regeneration. Since their first description, SCs were simply considered myogenic precursors, but now it is widely accepted that SCs are a heterogeneous stem cell population characterized by plasticity and self-renewal. In this report we focus on SCs capacity to undergo adipogenic differentiation both spontaneous and induced by adipogenic factors. Understanding SC behavior is especially important because their adipogenic potential could represent a pathophysiological explanation for the intramuscular fat depots and associated insulin resistance that characterize many metabolic diseases and age-related sarcopenia. Moreover, SC are a therapeutic promise for neuromuscular diseases in the context of tissue engineering, representing an interesting cell source for implantation.