Gluconeogenesis in dairy cows: The secret of making sweet milk from sour dough

Abstract

SummaryGluconeogenesis is a crucial process to support glucose homeostasis when nutritional supply with glucose is insufficient. Because ingested carbohydrates are efficiently fermented to short-chain fatty acids in the rumen, ruminants are required to meet the largest part of their glucose demand by de novo genesis after weaning. The qualitative difference to nonruminant species is that propionate originating from ruminal metabolism is the major substrate for gluconeogenesis. Disposal of propionate into gluconeogenesis via propionyl-CoA carboxylase, methylmalonyl-CoA mutase, and the cytosolic form of phosphoenolpyruvate carboxykinase (PEPCK) has a high metabolic priority and continues even if glucose is exogenously supplied. Gluconeogenesis is regulated at the transcriptional and several posttranscriptional levels and is under hormonal control (primarily insulin, glucagon, and growth hormone). Transcriptional regulation is relevant for regulating precursor entry into gluconeogenesis (propionate, alanine and other amino acids, lactate, and glycerol). Promoters of the bovine pyruvate carboxylase (PC) and PEPCK genes are directly controlled by metabolic products. The final steps decisive for glucose release (fructose 1,6-bisphosphatase and glucose 6-phosphatase) appear to be highly dependent on posttranscriptional regulation according to actual glucose status. Glucogenic precursor entry, together with hepatic glycogen dynamics, is mostly sufficient to meet the needs for hepatic glucose output except in high-producing dairy cows during the transition from the dry period to peak lactation. Lactating cows adapt to the increased glucose requirement for lactose production by mobilization of endogenous glucogenic substrates and increased hepatic PC expression. If these adaptations fail, lipid metabolism may be altered leading to fatty liver and ketosis. Increasing feed intake and provision of glucogenic precursors from the diet are important to ameliorate these disturbances. An improved understanding of the complex mechanisms underlying gluconeogenesis may further improve our options to enhance the postpartum health status of dairy cows.

Changes in milk performance and hepatic metabolism in mid-lactating dairy goats after being fed a high concentrate diet for 10 weeks

“…The liver controls metabolism and is responsible for nutrient partitioning as well as for supplying energy through gluconeogenesis and FA oxidation (Bobe et al, 2004;Aschenbach et al, 2010;Sejersen et al, 2012). In the present study, the hepatic concentrations of ATP and NAD were significantly increased in the HC group, which may indicate a sufficient energy supply in the liver.…”

Supplementation of conjugated linoleic acid in dairy cows reduces endogenous glucose production during early lactation

“…In ruminants, very little glucose originates from net portal absorption, and endogenous glucose production (eGP); that is, the sum of gluconeogenesis and glycogenolysis, provides most of the glucose for milk production (Danfaer, 1994;Bell and Bauman, 1997;Brockman, 2005;Aschenbach et al, 2010). Therefore, hepatic glucose production strongly increases after calving in dairy cows to provide glucose (Danfaer, 1994;Bell and Bauman, 1997;Brockman, 2005;Aschenbach et al, 2010). However, it is not known if CLA supplementation affects eGP as well as glucose oxidation (GOx) in high-yielding dairy cows during early lactation.…”

Relaciones entre calcio, ácidos grasos no esterificados, e insulina sanguínea en preparto y leche bovina perdida en el inicio de la lactancia

“…Sin embargo, en dicha acción también participa el ßHB (Zarrin et al 2013). La baja actividad de las enzimas gluconeogénicas y la baja tasa gluconeogénica posparto son las razones principales de la baja concentración de glucosa en plasma (Aschenbach et al 2010).…”