Background Adipose tissue expands in response to excess caloric intake, but individuals prone to deposit visceral (VIS) instead of subcutaneous (SQ) adipose tissue have higher risk of metabolic disease. The role of angiogenesis in the expandability of human adipose tissue depots is unknown. The objective of this study was to measure angiogenesis in VIS and SQ adipose tissue, and to establish whether there is a relationship between obesity, metabolic status and the angiogenic properties of these depots. Methods and results Angiogenic capacity was determined by quantifying capillary branch formation from human adipose tissue explants embedded in Matrigel, and capillary density was assessed by immunohistochemistry. SQ adipose tissue had a greater angiogenic capacity compared to VIS, even after normalization to its higher initial capillary density. Gene array analyses revealed significant differences in expression of angiogenic genes between depots, including an increased SQ expression of ANGPTL4, which is pro-angiogenic in an adipose tissue context. SQ capillary density and angiogenic capacity decreased with morbid obesity, and SQ, but not VIS, adipose tissue angiogenic capacity negatively correlated with insulin sensitivity. Conclusions These data imply that SQ adipose tissue has a higher capacity to expand its capillary network compared to VIS, but this capacity decreases with morbid obesity. The decrease correlates with insulin resistance, suggesting that impairment of SQ adipose tissue angiogenesis may contribute to metabolic disease pathogenesis.

Aims/hypothesis Recent reports of decreased capillary density in the adipose tissue of obese individuals suggest that an imbalance of angiogenesis and adipogenesis may, in part, underlie insulin resistance. This study aimed to determine whether the insulin-sensitising peroxisome proliferator-activated receptor γ (PPARγ) activator rosiglitazone affects adipose tissue vascularisation in normal humans. Methods A randomised, parallel-group, investigator-blinded placebo-controlled trial was conducted with normoglycaemic volunteers with BMI 27–43, recruited from the community at the University of Massachusetts Medical School, Worcester, MA, USA. Peri-umbilical adipose tissue biopsies were obtained before and after treatment for 6 weeks with rosiglitazone (8 mg once daily) or placebo, which were randomly allocated from a sequentially numbered list. The primary outcomes were adipocyte size and capillary density measured by immunohistochemistry, and angiogenic potential assessed by capillary sprout formation in Matrigel. Secondary outcomes were serum adiponectin, glycaemic, lipid and liver function variables. Results A total of 35 individuals fulfilling the inclusion criteria were randomised, and complete before-vs-after analyses were achieved in 30 participants (13 and 17, placebo and rosiglitazone, respectively). Significant differences, assessed by paired two-tailed Student t tests, were seen in response to rosiglitazone for adipocyte size (3,458±202 vs 2,693±223 μm2, p=0.0049), capillary density (5.6±0.5 vs 7.5±0.5 lumens/field, p=0.0098), serum adiponectin (14.3±1.5 vs 28.6±3.0 ng/ml, p<0.0001) and alkaline phosphatase (1.04±0.07 vs 0.87±0.05 μkat/l, p=0.001). A difference in angiogenic potential before and after treatment between the placebo and rosiglitazone groups was also seen (−23.88±14 vs 13.42±13, p=0.029, two-tailed Mann–Whitney test). Conclusions/interpretation Significant effects on adipose tissue vascular architecture occur after a short period of treatment with rosiglitazone in individuals with normal glucose tolerance. Improved adipose tissue vascularisation may, in part, mediate the therapeutic actions of this class of drugs.

Objective To describe the successful treatment of severe noninsulinoma hyperinsulinemic hypoglycemia with use of a calcium channel blocking agent in an adult patient who had previously undergone a gastric bypass surgical procedure. Methods A 65-year-old woman who had undergone a gastric bypass surgical procedure 26 years earlier was hospitalized because of severe postprandial hypoglycemia. During and after hospitalization, the patient underwent assessment with conventional measurements of glucose, insulin, proinsulin, and C-peptide; toxicologic studies; magnetic resonance imaging studies of the pancreas; and determination of hepatic vein insulin concentrations after selective splanchnic artery calcium infusion. Results Metabolic variables were consistent with the diagnosis of hyperinsulinemic hypoglycemia. Magnetic resonance imaging revealed the presence of a side branch intraductal papillary mucinous tumor that had been stable for more than 1 year. The results of the calcium-stimulated insulin release study were consistent with nonlocalized hypersecretion of insulin. A trial of frequent small feedings failed to prevent hypoglycemia. On the basis of reports of successful treatment of childhood nesidioblastosis, the patient was then prescribed nifedipine, 30 mg daily. She has subsequently remained free of symptomatic hypoglycemia for 20 months. Conclusion A calcium channel blocking agent may be efficacious and a potential alternative to partial pancreatectomy in cases of noninsulinoma hyperinsulinemic hypoglycemia in adults.

In recent years, the approach to understanding the hemodynamic norm has changed [17], however, to date, there are studies in which the authors use the average indicators obtained in the control group [2, 31].

Lung surfactant system, according to modern views, is a multicomponent, complex, self-regulating system, in which there are 3 main components: the surfactant itself - a thin lipoproteid film located at the air-liquid interface, hypophase and a cellular component represented by alveolocytes of types I, II, III. Lung surfactant system provides stability of alveoli during breathing, supports normal permeability of aerohematic barrier, participates in regulation of water balance, and has a protective function. Surface-active components of surfactant system are phospholipids, and more precisely their fraction - phosphatidylcholine.