DairyTransition CowMetabolic Support

GLUCOPLUS™ Glucose Precursor for Transition Dairy Cows

Give fresh cows a head start on glucose.

GLUCOPLUS™ is a coarse-powder supplement for the weeks around calving. It brings together three glucose precursors (propylene glycol, glycerol and calcium propionate) with niacin and cobalt, so the cow has more to work with when her intake drops and her milk production takes off.

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~30%drop in feed intake over the last three weeks before calving
3 + 2three glucose precursors, plus niacin and cobalt to keep the pathways running
250 / 300 gper cow per day, before and after calving
Intake figure from the transition-cow literature. Not a GLUCOPLUS™ trial result.

Around Calving, Glucose Gets Scarce

Within days of calving, the udder starts pulling in glucose to make lactose, and the cow's demand rises several-fold [1,2]. At the same time, she is eating less. Intake falls by about 30% over the last three weeks before calving [3]. To cover the gap, she breaks down body fat. That works for a while, but it has a price:

  • Ketosis. When the liver can't keep up with the fat coming in, ketone bodies pile up. In a multi-herd field study, subclinical ketosis (BHB of 1.2 mmol/L or more) was common in the first weeks of lactation [4].
  • Fatty liver. The liver takes up NEFA in proportion to what is released. What it can't burn or export is stored as triglyceride [6].
  • Lost production. Hyperketonemia goes hand in hand with more displaced abomasums, less milk and poorer fertility [5,7].

Propionate is the cow's main source of glucose, and a cow that eats less makes less of it [8]. So, the practical answer is to hand her glucose precursors directly and to keep the pathways that use them running. That is the thinking behind GLUCOPLUS™.

How it works

Three Precursors, Two Helpers, One Product

01

Give the liver more to make glucose from.

02

Keep propionate moving.

03

Ease the fat load on the liver.

JobComponentsWhat happens
Supply glucose precursorsPropylene glycol, glycerol, calcium propionateEach is absorbed or turned into propionate, and the liver uses it to make glucose [9,10,14].
Keep propionate movingCobalt sulfateRumen microbes need cobalt to make vitamin B12, which the cow needs to turn propionate into glucose [8,23].
Slow fat releaseNiacinActs on fat tissue to reduce lipolysis, so less NEFA reaches the liver [20,21].
Add calcium at calvingCalcium propionateBrings calcium and a glucose precursor together, just when calcium demand peaks [17,18,19].

Who does what?

TargetMain componentsMain mechanism
Blood glucosePropylene glycol, glycerol, calcium propionateGluconeogenesis in the liver from PG, glycerol and propionate
Blood NEFA and BHBPropylene glycol, niacinHigher glucose and insulin; less lipolysis [11,20]
Liver fatAll components, indirectlyLess NEFA reaches the liver; more propionate goes to glucose [6]
Propionate useCobalt sulfateVitamin B12 made by rumen microbes [23,25]

Why combine them?

Each precursor takes a different route into glucose metabolism. Propylene glycol is mostly absorbed as it is, and part is turned into propionate in the rumen [9,10]. Glycerol is absorbed too, and part is fermented to propionate [14]. Calcium propionate supplies propionate directly. Niacin and cobalt don't make glucose themselves. They deal with two common bottlenecks: too much fat release, and too little vitamin B12 for propionate metabolism.

The science

Where It All Meets: The TCA Cycle in the Cow's Liver

Everything GLUCOPLUS™ does comes back to one hub: the TCA cycle (also called the Krebs or citric acid cycle) inside liver mitochondria. The cycle burns acetyl-CoA for energy, and it also supplies the oxaloacetate that the liver turns into glucose [27].

A cow absorbs very little glucose from her gut. Most of her glucose is made in the liver from propionate, lactate, amino acids and glycerol [8,26]. Propionate is the largest single source. It becomes succinyl-CoA, joins the cycle at that point, runs on to oxaloacetate and leaves as glucose [8].

The TCA cycle in the cow's liver and where propionate, pyruvate, glycerol, niacin and cobalt feed in
Figure 1. The TCA cycle in the cow's liver and where the components of GLUCOPLUS™ feed in (schematic, after [8,27]).

How each component connects to the cycle

Calcium propionatePropionate becomes methylmalonyl-CoA and then succinyl-CoA, which enters the cycle and is carried through to oxaloacetate [8].
Cobalt sulfateCobalt is needed for vitamin B12. B12 is the cofactor of methylmalonyl-CoA mutase, the step that moves propionate into the cycle [8,23].
Propylene glycolMostly converted to lactate and pyruvate in the liver, and pyruvate carboxylase turns pyruvate into oxaloacetate. Part is fermented to propionate in the rumen first [9,10].
GlycerolEnters gluconeogenesis as glycerol-3-phosphate and DHAP, above the cycle. It makes glucose without using up cycle intermediates [27].
NiacinThe precursor of NAD⁺, the cofactor of the cycle's dehydrogenases (isocitrate, α-ketoglutarate and malate). It also slows fat release from adipose tissue [20,27].

Why oxaloacetate matters for ketosis

Oxaloacetate is needed twice: to take up acetyl-CoA and start the cycle, and to be turned into glucose. When glucose demand is high and propionate is short, the liver pulls oxaloacetate toward glucose. Fatty acids keep arriving and are broken down to acetyl-CoA, the cycle can't take it all, and the excess goes to ketone bodies [7,8]. This is the classic explanation. It is a simplification, because the energy and redox state of the liver also matter [8]. Still, more propionate and pyruvate coming in means more oxaloacetate available for both jobs.

A note on safety. Propylene glycol is generally recognized as safe by the U.S. FDA for use in animal feed. Cobalt from the whole ration should stay well under the maximum tolerable level of 25 mg/kg DM [24]. The requirement is only about 0.11 mg/kg DM [23].
Evidence

Glucose Precursors and Ketosis Control

Research on the individual components shows [9,11,13,20]:

Higher glucose and insulinOral propylene glycol raised plasma glucose and insulin in controlled trials [11].
Lower NEFA and ketonesPropylene glycol lowered plasma NEFA and BHB in early lactation cows [9].
A proven treatmentPropylene glycol is the most widely used oral treatment for ketosis in dairy cows [9,13].
Less lipolysisNiacin reduces NEFA release from fat tissue. How well it works depends on dose and delivery form [20,21,22].

Glucose Precursors and Liver Health

Fatty liver starts when more NEFA arrives than the liver can burn or export [6]. Anything that raises glucose and insulin and lowers NEFA goes after the cause:

Less fat coming inLower circulating NEFA means a lighter load on the liver [6,20].
Start before calvingPropylene glycol has been tested before calving specifically for fatty liver [12].
More propionate to glucoseCalcium propionate and cobalt support the main route for glucose synthesis in the ruminant liver [8].

GLUCOPLUS™ Glucose Precursor for Transition Dairy Cows

How a cow gets through the transition decides how she performs for the rest of the lactation. Metabolic disease costs milk, fertility and cows. GLUCOPLUS™ puts established glucose precursors together with niacin and cobalt to support her through calving and early lactation.

Products are not available in all countries. Permitted feeding levels may differ by region. Please contact your Filiz sales representative for details.

GLUCOPLUS™ Glucose Precursor

A coarse-powder glucose precursor for transition dairy cows, carried on corn cob. It combines propylene glycol, glycerol and calcium propionate with niacin and cobalt sulfate.

Dairy Cows
Active ingredientsPropylene glycol, glycerol, calcium propionate, niacin, cobalt sulfate
FormCoarse powder on a corn cob carrier
Pack size20 kg
Shelf life6 months from production date
StorageCool, dry place away from sunlight and moisture.

Recommended intake

StageRecommended intake
Before calving (close-up dry cows)250 g per cow per day
After calving (fresh cows)300 g per cow per day

Feeding instructions: Mix evenly into the ration or top-dress at feeding. Check that total calcium and cobalt intake from all sources stays within requirements and maximum levels. Ask your regional nutritionist for the final feeding level.

Resources

GLUCOPLUS™ Research at a Glance

What the literature says about each component

ComponentKey pointsRefs
Propylene glycolAbsorbed from the rumen and turned into glucose by the liver; part is fermented to propionate. Raises glucose and insulin, lowers NEFA and BHB. The standard oral treatment for ketosis.9–13
GlycerolAbsorbed from the rumen and used for gluconeogenesis; part is fermented to propionate. Results vary between trials.14–16
Calcium propionateSupplies propionate and calcium at calving. Used to prevent hypocalcemia and as an energy source.17–19
NiacinInhibits lipolysis and lowers plasma NEFA. The effect can be followed by a rebound and depends on dose and form.20–22
CobaltNeeded for ruminal vitamin B12 synthesis. Requirement about 0.11 mg/kg DM; maximum tolerable level 25 mg/kg DM.23–25

These are published studies on the individual components. They are not GLUCOPLUS™ trial results.

Planning Your Transition Program with GLUCOPLUS™?

Tell us about your herd, your close-up and fresh-cow rations and your metabolic disease records. Our technical team will help you build a feeding plan that fits.

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Sources (27 references)
  1. Bell AW. Regulation of organic nutrient metabolism during transition from late pregnancy to early lactation. J Anim Sci. 1995;73:2804–2819.
  2. Drackley JK. Biology of dairy cows during the transition period: the final frontier? J Dairy Sci. 1999;82:2259–2273.
  3. Grummer RR. Impact of changes in organic nutrient metabolism on feeding the transition dairy cow. J Anim Sci. 1995;73:2820–2833.
  4. McArt JAA, Nydam DV, Oetzel GR. Epidemiology of subclinical ketosis in early lactation dairy cattle. J Dairy Sci. 2012;95:5056–5066.
  5. Duffield TF, Lissemore KD, McBride BW, Leslie KE. Impact of hyperketonemia in early lactation dairy cows on health and production. J Dairy Sci. 2009;92:571–580.
  6. Bobe G, Young JW, Beitz DC. Pathology, etiology, prevention, and treatment of fatty liver in dairy cows. J Dairy Sci. 2004;87:3105–3124.
  7. Herdt TH. Ruminant adaptation to negative energy balance: influences on the etiology of ketosis and fatty liver. Vet Clin North Am Food Anim Pract. 2000;16:215–230.
  8. Aschenbach JR, Kristensen NB, Donkin SS, Hammon HM, Penner GB. Gluconeogenesis in dairy cows: the secret of making sweet milk from sour dough. IUBMB Life. 2010;62:869–877.
  9. Nielsen NI, Ingvartsen KL. Propylene glycol for dairy cows: a review of the metabolism of propylene glycol and its effects on physiological parameters, feed intake, milk production and risk of ketosis. Anim Feed Sci Technol. 2004;115:191–213.
  10. Kristensen NB, Raun BM. Ruminal and intermediary metabolism of propylene glycol in lactating Holstein cows. J Dairy Sci. 2007;90:4707–4717.
  11. Grummer RR, Winkler JC, Bertics SJ, Studer VA. Effect of propylene glycol dosage during feed restriction on metabolites in blood of prepartum Holstein heifers. J Dairy Sci. 1994;77:3618–3623.
  12. Studer VA, Grummer RR, Bertics SJ. Effect of prepartum propylene glycol administration on periparturient fatty liver in dairy cows. J Dairy Sci. 1993;76:2931–2939.
  13. McArt JAA, Nydam DV, Ospina PA, Oetzel GR. A field trial on the effect of propylene glycol on milk yield and resolution of ketosis in fresh cows diagnosed with subclinical ketosis. J Dairy Sci. 2011;94:6011–6020.
  14. Rémond B, Souday E, Jouany JP. In vitro and in vivo fermentation of glycerol by rumen microbes. Anim Feed Sci Technol. 1993;41:121–132.
  15. DeFrain JM, Hippen AR, Kalscheur KF, Jardon PW. Feeding glycerol to transition dairy cows: effects on blood metabolites and lactation performance. J Dairy Sci. 2004;87:4195–4206.
  16. Chung YH, Rico DE, Martinez CM, et al. Effects of feeding dry glycerin to early postpartum Holstein dairy cows on lactational performance and metabolic profiles. J Dairy Sci. 2007;90:5682–5691.
  17. Goff JP, Horst RL. Oral administration of calcium salts for treatment of hypocalcemia in cattle. J Dairy Sci. 1993;76:101–108.
  18. Pehrson B, Svensson C, Jonsson M. A comparative study of the effectiveness of calcium propionate and calcium chloride for the prevention of parturient hypocalcemia in dairy cows. J Dairy Sci. 1998;81:2011–2016.
  19. Stokes SR, Goff JP. Evaluation of calcium propionate and propylene glycol administered into the esophagus of dairy cattle at calving. Prof Anim Sci. 2001;17:115–122.
  20. Niehoff ID, Hüther L, Lebzien P. Niacin for dairy cattle: a review. Br J Nutr. 2009;101:5–19.
  21. Pires JAA, Grummer RR. The use of nicotinic acid to induce sustained low plasma nonesterified fatty acid concentrations in feed-restricted Holstein cows. J Dairy Sci. 2007;90:3725–3732.
  22. Morey SD, Mamedova LK, Anderson DE, Armendariz CK, Titgemeyer EC, Bradford BJ. Effects of encapsulated niacin on metabolism and production of periparturient dairy cows. J Dairy Sci. 2011;94:5090–5104.
  23. National Research Council. Nutrient Requirements of Dairy Cattle. 7th rev. ed. Washington, DC: National Academies Press; 2001.
  24. National Research Council. Mineral Tolerance of Animals. 2nd rev. ed. Washington, DC: National Academies Press; 2005.
  25. Kincaid RL, Socha MT. Effect of cobalt supplementation during late gestation and early lactation on milk and serum measures. J Dairy Sci. 2004;87:1813–1816.
  26. Young JW. Gluconeogenesis in cattle: significance and methodology. J Dairy Sci. 1977;60:1–15.
  27. Nelson DL, Cox MM. Lehninger Principles of Biochemistry. 8th ed. New York: W.H. Freeman; 2021.