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Changes in faecal bacteria and metabolic parameters in foals during the first six weeks of life
(2011)
Many foals develop diarrhoea within the first two weeks of life which has been suggested to coincide with postpartum oestrus in their dams. To analyse the pathogenesis of this diarrhoea we have determined faecal bacteria in foals and their dams (n = 30 each), and serum IGF-1 and gamma-globulins for 6 weeks after birth. In addition, effects of beta-carotene supplementation to mares (group 1: 1000 mg/day, n = 15, group 2: control, n = 15) on diarrhoea in foals were studied. Diarrhoea occurred in 92 and 79% of foals in groups 1 and 2, respectively, but was not correlated with oestrus in mares. Beta-carotene supplementation was without effect on foal diarrhoea. In mares, bacterial flora remained stable. The percentage of foals with cultures positive for E. coli was low at birth but increased within one day, the percentage positive for Enterococcus sp. was low for 10 days and for Streptococcus sp. and Staphylococcus sp. was low for 2-4 weeks. By 4 weeks of age, bacterial flora in foals resembled an adult pattern. Concentration of serum IGF-1 was low at birth (group 1:149 +/- 11, group 2:166 17 ng/ml), increased after day 1 (day 7 group 1:384 +/- 30, group 2: 372 +/- 36) but at no time differed between groups. Serum gamma-globulin concentration in foals was low before colostrum intake and highest on day 1 (p < 0.001 over time). In conclusion, neonatal diarrhoea in foals does not coincide with postpartum oestrus in their dams but with changes in intestinal bacteria and is not influenced by beta-carotene supplementation given to mares.
The relationship between nutrition and the development of chronic diseases including metabolic syndrome, diabetes mellitus, cancer and cardiovascular disease has been well studied. On the other hand, changes in the GH-IGF-1 axis in association with nutrition-related diseases have been reported. The interplay between GH, total IGF-1 and different inhibitory and stimulatory kinds of IGF-1 binding proteins (IGFBPs) results in IGF-1 bioactivity, the ability of IGF-1 to induce phosphorylation of its receptor and consequently its signaling. Moreover, IGF-1 bioactivity is sufficient to reflect any change in the GH-IGF-1 system. Accumulating evidence suggests that both of high protein diet, characterized by increased glucagon secretion, and insulin-induced hypoglycemia increase mortality rate and the mechanisms are unclear. However both of glucagon and insulin-induced hypoglycemia are potent stimuli of GH secretion. The aim of the current study was to identify the impact of glucagon and insulin-induced hypoglycemia on IGF-1 bioactivity as possible mechanisms. In a double-blind placebo-controlled study, glucagon was intramuscularly administrated in 13 type 1 diabetic patients (6 males /7 females; [BMI]: 24.8 ± 0.95 kg/m2), 11 obese subjects (OP; 5/ 6; 34.4 ± 1.7 kg/m2), and 13 healthy lean participants (LP; 6/ 7; 21.7 ± 0.6 kg/m2), whereas 12 obese subjects (OP; 6/ 6; 34.4 ± 1.7 kg/m2), and 13 healthy lean participants (LP; 6/ 7; 21.7 ± 0.6 kg/m2) performed insulin tolerance test in another double-blind placebo-controlled study and changes in GH, total IGF-1, IGF binding proteins (IGFBPs) and IGF-1 bioactivity, measured by the cell-based KIRA method, were investigated. In addition, the interaction between the metabolic hormones (glucagon and insulin) and the GH-IGF-1 system on the transcriptional level was studied using mouse primary hepatocytes. In this thesis, glucagon decreased IGF-1 bioactivity in humans independently of endogenous insulin levels, most likely through modulation of IGFBP-1 and-2 levels. The glucagon-induced reduction in IGF-1 bioactivity may represent a novel mechanism underlying the impact of glucagon on GH secretion and may explain the negative effect of high protein diet related to increased cardiovascular risk and mortality rate. In addition, insulin-induced hypoglycemia was correlated with a decrease in IGF-1 bioactivity through up-regulation of IGFBP-2. These results may refer to a possible and poorly explored mechanism explaining the strong association between hypoglycemia and increased cardiovascular mortality among diabetic patients.