The periparturient period in dairy cows is associated with alterations in insulin action in peripheral tissues; however, the molecular mechanism underlying this process is not completely understood. The objective was to examine the response to a glucose tolerance test (GTT) and to analyze insulin signaling in liver and adipose tissues in pre- and postpartum dairy cows. Liver and adipose tissue biopsies were taken before and after GTT, at 17d prepartum and again at 3 to 5d postpartum from 8 high-yielding Israeli Holstein dairy cows. Glucose clearance rate after GTT was similar pre- and postpartum. Basal insulin concentrations and the insulin response to GTT were approximately 4-fold higher prepartum than postpartum. In accordance, phosphorylation of the hepatic insulin receptor after GTT was higher prepartum than postpartum. Across periods, a positive correlation was observed between the basal and peak plasma insulin and phosphorylated insulin receptor after GTT in the liver. Hepatic phosphorylation of protein kinase B after GTT was elevated pre- and postpartum. Conversely, in adipose tissue, phosphorylation of protein kinase B after GTT pre- and postpartum was increased only in 4 out of 8 cows that lost less body weight postpartum. Our results demonstrate that hepatic insulin signaling is regulated by plasma insulin concentrations as part of the homeorhetic adjustments toward calving, and do not support a model of hepatic insulin resistance in periparturient cows. Nevertheless, we suggest that specific insulin resistance in adipose tissue occurs pre- and postpartum only in cows prone to high weight loss. The different responses among these cows imply that genetic background may affect insulin responsiveness in adipose tissue pre- and postpartum.

Disturbance in metallochemical reactions and metal‐protein association are associated with chronic neurodegenerative conditions, such as Alzheimer's and Parkinson's disease, as well as with neurodegeneration triggered by acute cerebral ischaemia. Many neurological diseases have been linked directly or indirectly to perturbed homeostasis of Ca, Fe, Zn, or Cu ions. Consequently, acute or chronic neurodegenerative disorders represent excellent targets for exploiting metal ion chelator approaches. Drug Dev. Res. 56: 300–309, 2002. © 2002 Wiley‐Liss, Inc.

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Calcium-binding protein D28K (calbindin) synthesis, vitamin D metabolism and shell quality were investigated in young and aged laying hens fed diets containing either cholecalciferol (CC) or its 1-hydroxylated derivatives. Duodenal calbindin concentration was similar in the young and in the aged laying hens. Exogenous 1-hydroxylated CC derivatives increased duodenal calbindin concentration, regardless of age. Shell weight and shell density (mg/cm2) were significantly lower (P less than 0.01) in the aged than in the young hens. Egg shell weight and density tended to decrease along the clutch. The rate of decline was higher in aged than in young hens. Feeding aged hens a diet containing 5 micrograms 1,25-dihydroxycholecalciferol [1,25(OH)2CC] or 1 alpha-hydroxycholecalciferol per kilogram improved shell quality, slowed down the progressive reduction in shell quality during the clutch and increased culling and mortality. The results indicate a) that the capacity for expression of 1,25(OH)2D3 in the intestine is not altered by age and b) that prolonged feeding of 1-hydroxylated derivatives of vitamin D3 improves shell quality in aged laying hens and increases culling and mortality.

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