Regulation of mammary glucose uptake in goats: role of mammary gland supply, insulin, IGF-1 and synthetic capacity

Citation
Mo. Nielsen et al., Regulation of mammary glucose uptake in goats: role of mammary gland supply, insulin, IGF-1 and synthetic capacity, J DAIRY RES, 68(3), 2001, pp. 337-349
Citations number
35
Categorie Soggetti
Food Science/Nutrition
Journal title
JOURNAL OF DAIRY RESEARCH
ISSN journal
00220299 → ACNP
Volume
68
Issue
3
Year of publication
2001
Pages
337 - 349
Database
ISI
SICI code
0022-0299(200108)68:3<337:ROMGUI>2.0.ZU;2-M
Abstract
Variations in mammary glucose uptake were measured during the normal pregna ncy-lactation cycle in dairy goats. In addition mammary glucose uptake was studied in response to somatotropin (ST) treatment in mid-lactation and acu te increases in glucose concentration induced by sodium-propionate challeng e in early lactation. Mammary glucose uptake was independent of arterial gl ucose, insulin ana Insulin-like Growth Factor-1 (IGF-1) concentrations duri ng lactation and during acute increases in arterial glucose concentration. Glucose uptake in the lactating mammary gland of the goat must therefore be carried out by an insulin-independent carrier, possible GLUT I, and glucos e supply is not a limiting factor for uptake under in vivo conditions. Extr action of glucose uptake changed markedly during the normal course of lacta tion, following the overall changes in milk yield. Concentrations of glucos e in skimmed milk, believed to reflect intracellular glucose concentration, changed in opposite directions, resulting in decreasing ratios of arterial : skimmed milk glucose concentration with progressing lactation. Thus, mamm ary synthetic capacity also involves a capacity for glucose uptake, which m ay be influenced by variations in glucose carrier numbers, as well as mamma ry metabolic activity (intracellular glucose concentration). In contrast to the situation during the normal course of lactation, ST stimulated milk yi eld, despite less efficient glucose extraction.