Developmental regulation of adipose tissue growth through hyperplasia and hypertrophy in the embryonic Leghorn and broiler

Abstract

The United States is a world leader in poultry production, which is the reason why achieving better performance and muscle growth each year is a necessity. Reducing accretion of adipose tissue is another important factor for poultry producers because this allows more nutrients to be directed toward muscle growth, but the effect of embryonic adipose growth on posthatch development has not been fully understood. The purpose of this study was to investigate the total DNA mass, morphological characteristics, differentiation markers, and triglyceride breakdown factors of embryonic adipose tissue, and their relation to hyperplastic and hypertrophic growth within layers (Leghorn) and meat-type chickens (broilers). After embryonic day (E) 12, broiler weight was significantly higher than Leghorn, and this trend continued throughout the rest of incubation and posthatch (P < 0.05). Neck and leg fat pad weights between the 2 breeds did not differ at most of the time points. A remarkable increase in total DNA mass was observed between E12 and E14 in both Leghorn and broilers (P < 0.05), indicating a high potential for hyperplastic growth during this time. Histological analysis revealed clusters of preadipocytes at E12; however, the majority of these cells differentiated by E14 and continued to grow until the time of hatch. The adipocyte sizes between both breeds did not generally differ, even though broilers are known to have larger adipocytes posthatch. Fatty acid-binding protein 4 expression levels in Leghorn and broilers continued to rise with each time point, which paralleled the expansion of mature adipocytes. Adipose triglyceride lipase was highly expressed at E20 and d 1 posthatch to mobilize triglyceride degradation for energy during hatching. Thus, embryonic chicken adipose tissue was found to develop by hyperplastic mechanisms followed by hypertrophy. At embryonic stages and early posthatch, layer- and meat-type chicken adipose growth does not differ, which suggests breed differences occur posthatch.

Overexpression of G0/G1 Switch Gene 2 in Adipose Tissue of Transgenic Quail Inhibits Lipolysis Associated with Egg Laying

“…All procedures, including dehydration, embedding, sectioning, and staining with hematoxylin and eosin, for the fixed adipose samples from non-transgenic and transgenic FG1 and FG3 quail were conducted in accordance with our previous report [ 24 ]. Images were captured with an AXIO-Vert.A1 optical microscope (Carl Zeiss Microscopy, Thornwood, NY, USA) furnished with an AxioCam MRc5 camera (Carl Zeiss Microscopy).…”

Research Note: Association of temporal expression of myostatin with hypertrophic muscle growth in different Japanese quail lines

“…Right after hatching, chicks before access to food have been under stressful conditions such as the hatching process which demands for high energy expenditure ( Lee et al., 2009 ). The chicks at D0 actively mobilize fatty acid from both adipose tissue and yolk to supply energy for survival ( Lee et al., 2009 , Chen et al., 2014 ). This stress condition causes a temporal halt in growth of the chicks that may inhibit expression of MSTN in PM of both RBC and HW lines ( Figures 2 B and 2 C).…”

Adipogenic and Myogenic Potentials of Chicken Embryonic Fibroblasts in vitro: Combination of Fatty Acids and Insulin Induces Adipogenesis

“…However, there is a lack of an avian in vitro model to better understand early adipogenic processes. In the current study, we developed a new in vitro method for adipocyte differentiation of CEF isolated from embryonic day 5, 6, and 7 when there is no visible fat tissue (Chen et al, ).…”