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Evidence for the involvement of a gastrointestinal peptide in the regulation of glucose uptake in the mammary gland of the lactating rat.

ABSTRACT: 1. A method of obtaining serial arterial and mammary-venous blood samples was used to identify possible factors involved in the regulation of glucose uptake in the gland of the lactating rat. 2. Administration of insulin alone increased the arteriovenous glucose difference across the mammary gland of starved rats, but the time course of the recovery could not account for the restoration of arteriovenous glucose difference observed during refeeding [Page & Kuhn (1986). Biochem. J. 239, 269-274]. 3. A crude extract of the gastrointestinal tract (stomach-ileum) from lactating rats enhanced the change in mammary glucose uptake observed with insulin, but only when large amounts (100 munits/rat) of insulin were used. To achieve a similar recovery of arteriovenous glucose difference using near-physiological amounts (5 munits/rat) of insulin it was necessary to sever the mammary nerves. 4. A peptide fraction (of less than 10 kDa) isolated from the gut extract enhanced the effect of insulin in a similar manner to the crude extract. 5. It is suggested that in addition to insulin at least another component, probably a gut peptide, is required for the restoration of mammary glucose uptake during refeeding. An inhibitory component may also contribute to the regulation of mammary glucose extraction in the lactating rat.

SUBMITTER: Page T

PROVIDER: S-EPMC1138414 | biostudies-other | 1989 Mar

REPOSITORIES: biostudies-other

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Project description:To investigate the role of glucose in regulating milk fatty acid synthesis, 6 lactating Guanzhong dairy goats were infused with 0, 60, or 100 g/d glucose via the external pubic artery in a 3 × 3 repeated Latin square experiment. A concomitant in vitro experiment was conducted to investigate possible mechanisms whereby glucose regulates milk fatty acid synthesis. RNA sequencing was used for cellular transcriptome analysis. Drugs, MK-2206, rapamycin, and dorsomorphin were used to block cellular mammalian AMP-activated protein kinase (AMPK), AKT serine/threonine kinase 1, and mechanistic target of rapamycin kinase signaling pathways, respectively. Carbohydrate response element binding protein (ChREBP) was knockdown and overexpressed to investigate its role in regulating milk fatty acid synthesis in mammary epithelial cells. Glucose infusion linearly elevated the concentration of C8:0 (P = 0.039) and C10:0 (P = 0.041) in milk fat while it linearly decreased (P = 0.049) that of C16:0. This result was in agreement with the upregulation of genes related to de novo synthesis of fatty acids and lipid droplet formation, including adipose differentiation-related protein, butyrophilin subfamily 1 member A1, fatty acid synthase (FASN) and ChREBP. Their expression increased (P < 0.05) linearly in the lactating goat mammary gland. In vitro, glucose linearly stimulated the expression of genes related to de novo synthesis of fatty acids and cellular triacylglycerol in cultured mammary epithelial cells. RNA sequencing and inhibition studies revealed that glucose induced transcriptomic changes increasing lipogenic pathways, with AMPK responding to glucose by controlling ChREBP and FASN. Knockdown and overexpression of ChREBP highlighted its essential role in lipogenesis. The knockdown and overexpression of ChREBP protein also revealed an essential role in regulating the de novo synthesis of fatty acids. Collectively, our data highlight that glucose supplementation promotes de novo fatty acid synthesis via the AMPK-ChREBP axis, hence increasing milk fat yield in the goat mammary gland. Results from the current study provide possible strategies to manipulate the fatty acid composition as well as improve ruminant milk quality.

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Evidence for the involvement of a gastrointestinal peptide in the regulation of glucose uptake in the mammary gland of the lactating rat.

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