Adipose Tissue Architecture and Gestational Weight Gain in Normoglycemic Pregnancies

Objective: To investigate histologic architecture of subcutaneous (SQAT) and visceral adipose tissue (VAT) growth in relationship to gestational weight gain (GWG). Epidemiological data suggest that SQAT expansion may be protective of obesity related co-morbidities, whereas VAT expansion is associated with Type-2 diabetes risk. We hypothesized that in normal gravidas, GWG would be associated with hypertrophy of SQAT and not VAT. Methods: A subset of subjects enrolled in the Pregnancy & Postpartum Observational Dietary Study (PPODS) and undergoing Cesarean delivery had SQAT (midline superior edge Pfannenstiel incision) and VAT (inferior omental periphery) biopsies after neonatal delivery, uterine closure and hemostasis achievement. Excised tissues were fixed and stained. Average adipocyte size and capillary density were assessed in 10 independent sections per AT depot per subject. GWG determined by the difference of weight at first visit and immediately postpartum (1-4 days post-op). GWG plotted vs mean SQAT or VAT adipocyte size. Results: Table illustrates general clinical characteristics of the 5 subjects. Figure A demonstrates SQAT and VAT mean adipocyte size with representative sections from patient E depicted above bar graphs representing means and SEM from 5 patients. SQ adipocytes were significantly larger than those from VAT. Significant positive correlation was noted between GWG and SQAT adipocyte size (Figure B), but not VAT adipocyte size (Figure C). Discussion: Preliminary results reveal that in normal pregnancies, GWG is associated with changes in SQAT but not VAT architecture, which reflects lipid accumulation. These results are consistent with the model that SQAT is specifically adapted for healthy lipid storage, and provides a basis for comparison between normal gravidas and those with GDM

Adipose tissue angiogenesis: impact on obesity and type-2 diabetes

The growth and function of tissues are critically dependent on their vascularization. Adipose tissue is capable of expanding many-fold during adulthood, therefore requiring the formation of new vasculature to supply growing and proliferating adipocytes. The expansion of the vasculature in adipose tissue occurs through angiogenesis, where new blood vessels develop from those pre-existing within the tissue. Inappropriate angiogenesis may underlie adipose tissue dysfunction in obesity, which in turn increases type-2 diabetes risk. In addition, genetic and developmental factors involved in vascular patterning may define the size and expandability of diverse adipose tissue depots, which are also associated with type-2 diabetes risk. Moreover, the adipose tissue vasculature appears to be the niche for pre-adipocyte precursors, and factors that affect angiogenesis may directly impact the generation of new adipocytes. Here we review recent advances on the basic mechanisms of angiogenesis, and on the role of angiogenesis in adipose tissue development and obesity. A substantial amount of data points to a deficit in adipose tissue angiogenesis as a contributing factor to insulin resistance and metabolic disease in obesity. These emerging findings support the concept of the adipose tissue vasculature as a source of new targets for metabolic disease therapies. This article is part of a Special Issue entitled: Modulation of Adipose Tissue in Health and Disease