HEAT STRESS AFFECTS INSULIN SENSITIVITY IN PRIMARY BOVINE ADIPOCYTES
Animals experiencing heat stress (HS) have diminished lipolytic response. Current research on lipid metabolism in lactating cows shows a clear disconnect between in vivo and in vitro data, wherein bovine cells cultured under HS conditions were found to be more sensitive to lipolytic stimuli. The objective of this study was to determine if HS affects insulin sensitivity in subcutaneous adipose tissue (AT) of dairy cattle. Bovine primary adipocytes, isolated from 7 multiparous Holstein cows in late lactation, were cultured at either 42°C (HS) or 37°C (thermal neutral, TN) and incubated with varying concentrations of insulin (0 – 2.5 mU) in combination with isoproterenol (ISOP, 10-6 M). Glycerol release was measured as an indicator of lipolytic response. The effects of temperature and insulin concentration, as well as their interaction on AT lipolysis were evaluated. Likewise, the abundance of several lipolytic proteins in relation to HS was analyzed. A significant insulin concentration by temperature interaction was observed in HS (P<0.001) but not TN (P=0.34) cells. Insulin significantly reduced the amount of glycerol released (P<0.001), indicating a decline in response to lipolytic stimuli. Meanwhile, in the absence of insulin, adipocytes cultured under HS exhibited an elevated response to ISOP (P<0.001) relative to their TN counterparts. Basal lipolytic (-ISOP/-insulin) response was not different between HS and TN cells (P>0.05). Furthermore, a significant decrease in the phosphorylation of hormone sensitive lipase (HSL) at Serine 563 (P=0.03) and perilipin (P=0.04) with respect to increasing insulin concentrations was observed for cells cultured under HS but not TN conditions. These data support the view that HS affects insulin sensitivity of bovine adipocytes, suggesting that HS may indirectly prevent in vivoadipose tissue mobilization as a result of heat-induced increase in circulating insulin concentrations, combined with higher AT sensitivity to insulin.
Keywords: heat stress, adipose tissue, insulin, lipolysis