Effect of dexamethasone, feeding time, and insulin infusion on leptin concentrations in stallions1

Abstract

Three experiments tested the hypotheses that daily cortisol rhythm, feeding time, and/or insulin infusion affect(s) leptin secretion in stallions. Ten mature stallions received ad libitum hay and water and were fed a grain concentrate once daily at 0700. In Exp. 1, stallions received either a single injection of dexamethasone (125 microg/kg BW i.m.; n = 5) or vehicle (controls; n = 5) at 0700 on d -1. Starting 24 h later, blood samples were collected every 2 h for 36 h via jugular venipuncture. Cortisol in control stallions varied (P < 0.01) with time, with a morning peak and evening nadir; dexamethasone suppressed (P < 0.01) cortisol concentrations. Leptin and insulin were greater (P < 0.01) in the treated stallions, as was the insulin response to feeding (P < 0.01). Leptin in control stallions varied (P < 0.01) in a diurnal pattern, peaking approximately 10 h after onset of eating. This pattern of leptin secretion was similar, although of greater magnitude (P < 0.01), in treated stallions. In Exp. 2, five stallions were fed the concentrate portion of their diet daily at 0700 and five were switched to feeding at 1900. After 14 d on these regimens, blood samples were collected every 4 h for 48 h and then twice daily for 5 d. Cortisol varied diurnally (P = 0.02) and was not altered (P = 0.21) by feeding time. Insulin and leptin increased (P < 0.01) after feeding, and the peaks in insulin and leptin were shifted 12 h by feeding at 1900. In Exp. 3, six stallions were used in two 3 x 3 Latin square experiments. Treatments were 1) normal daily meal at 0700; 2) no feed for 24 h; and 3) no feed and a bolus injection of insulin (0.4 mIU/kg BW i.v.) followed by infusion of insulin (1.2 mIU.kg BW(-1).min(-1)) for 180 min, which was gradually decreased to 0 by 240 min; sufficient glucose was infused to maintain euglycemia. Plasma insulin increased (P < 0.01) in stallions when they were meal-fed (to approximately 150 microIU/mL) or infused with insulin and glucose (to approximately 75 microIU/mL), but insulin remained low (10 microIU/mL or less) when they were not fed. The increases in insulin were paralleled by gradual increases (P < 0.01) in leptin concentrations 3 to 4 h later in stallions fed or infused with insulin and glucose. When stallions were not fed, leptin concentrations remained low. These results demonstrate that feeding time, and more specifically the insulin increase associated with a meal, not cortisol rhythm, drives the postprandial increase in plasma leptin concentrations in horses.

Prediction of incipient pasture‐associated laminitis from hyperinsulinaemia, hyperleptinaemia and generalised and localised obesity in a cohort of ponies

“…Leptin is primarily produced and secreted from adipose tissue at levels that are proportional to body condition (Buff et al 2002); and its secretion is stimulated by insulin and inversely related to insulin sensitivity in obese horses (Cartmill et al 2003(Cartmill et al , 2005Frank et al 2006). Additionally, obesity is related to a state of relative insulin resistance (Hoffman et al 2003;Vick et al 2007), with adipose tissue deposited specifically along the crest of the neck associated with insulin concentration or glucose tolerance (Frank et al 2006;Carter et al 2008).…”

Long-Term Dexamethasone Exposure Down-Regulates Hepatic TFR1 and Reduces Liver Iron Concentration in Rats

“…However, the 7-day or 14-day psychological stress exposure induced by the communication box did not affect food intake and body weight [13,35,36]. Long-term and severe stress results in inhibition of growth and food intake, in part because the increasing release of leptin functions as feeding reductions and enhances energy output [23,37,38]. …”

Obesity

“…Weyenberg et al 2008a) and increases following meal feeding (Cartmill et al 2005). The insulin increase associated with meal feeding appears to drive the postprandial increase in plasma leptin (Cartmill et al 2005).…”

“…The insulin increase associated with meal feeding appears to drive the postprandial increase in plasma leptin (Cartmill et al 2005). Dexamethasone administration has also been shown to be a potent stimulator of leptin secretion in horses, whereas physiological elevation of cortisol concentrations following ACTH administration produced only minor increases in leptin (Cartmill et al 2005).…”

“…Plasma leptin concentration in horses is affected by energy balance and feeding state (McManus & Fitzgerald 2000, Cartmill et al 2005. Higher plasma leptin concentrations were reported in fed horses compared with fasted horses, with higher values in the afternoon than the morning only in the fed horses .…”