The paper
Fat deposition in ruminants
- Author
- E.F. Annison
- Published
- 1993
- In
- Recent Advances in Animal Nutrition in Australia
- Collection
- RAAN proceedings
- Listed on the old library
- 1 February 2012
We know of no online copy of this paper today. A university or state library that holds the Recent Advances in Animal Nutrition in Australia is the place to ask.

In this summary
- The question behind fat deposition in ruminants
- How fat cells grow and where fat is made
- Acetate, not glucose, fuels ruminant fat synthesis
- What happens to dietary fat and why the rumen limits it
- Protecting fat from the rumen to change meat composition
- Breeding for late maturity: the most reliable lever
- Hormones, agonists and the push toward immunological tools
- Sources and further reading
- Questions
The question behind fat deposition in ruminants#
Fat accompanies growth in any meat animal, but by the early 1990s consumer demand for leaner meat had pushed researchers to look harder at how that fat gets laid down, and where it could be limited without undermining weight gain. Annison's review draws together work on adipose tissue biology, hormonal control and the practical tools available to producers, from feeding and breeding choices through to growth promotants and emerging immunological methods.
The paper is not a single experiment but a synthesis of findings from sheep, cattle and some non-ruminant comparisons, drawing on sources ranging from biochemical studies of fatty acid synthesis to production trials with growth hormone and beta-adrenergic agonists. It sits within the RAAN Conference Proceedings series, a collection of applied nutrition papers presented to Australian scientists and advisers; the full set of papers from that community is available through the Recent Advances in Animal Nutrition collection, which is also indexed on the RAAN Conference Proceedings page of this index.
How fat cells grow and where fat is made#
Adipose tissue is distributed across the body as discrete depots, and the paper notes that, contrary to earlier assumptions, fat growth at every stage involves both an increase in cell numbers (hyperplasia) and an increase in cell size (hypertrophy), both of which can be shifted by nutrition. New fat cells arise from undifferentiated cells in the stromal-vascular fraction of adipose tissue, and these can be grown in culture.
Adams and colleagues isolated these precursor cells from different fat depots of sheep of varying ages and found no detectable differences in how fast they grew under optimal culture conditions, suggesting the cells themselves are not intrinsically programmed to grow at different rates depending on their depot of origin. Growth responses to various hormones and growth factors also did not line up with the depot the cells came from.
Yet whole depots clearly behave differently in the live animal. Van der Walt, cited in the review, reported that the manufacture of long-chain fatty acids from scratch is markedly higher in backfat than in mesenteric fat, and that the relative activity of different depots can shift with age, nutrition and physiological state. The paper does not resolve why cells that seem interchangeable in culture end up behaving so differently once embedded in different depots of the live animal.
Acetate, not glucose, fuels ruminant fat synthesis#
One of the clearest biochemical points in the paper is that ruminants build fatty acids from acetate rather than glucose, the reverse of the pattern in non-ruminants. This is explained by low activity in ruminant tissue of the enzyme pathways that would normally shuttle glucose-derived carbon into fat synthesis, along with reduced glycolytic enzyme activity.
Fat synthesis also needs a supply of reducing power in the form of NADPH. In non-ruminants this mostly comes from glucose breakdown via the pentose phosphate pathway and paired malate dehydrogenase enzymes; in ruminants, the paper explains, that second source is largely missing, and the isocitrate dehydrogenase pathway handling acetate, together with pentose cycle activity, appears to fill the gap.
Lactate and pyruvate both contribute some carbon to fat synthesis in ruminant adipose tissue, while propionate and methylmalonate contribute only slightly under normal diets. Annison notes that on diets that sharply raise the proportion of propionate among rumen volatile fatty acids, sheep and goats can accumulate odd-numbered and branched-chain fatty acids making up 10.20% of depot fat, a reminder that diet composition reaches right down into the chemical make-up of stored fat.
What happens to dietary fat and why the rumen limits it#
Green herbage and cereal grain both carry a modest proportion of lipid on a dry matter basis, the paper notes, with herbage lipid mostly in the form of galactolipids and cereal lipid mainly as triacylglycerol; both sources are rich in C-18 unsaturated fatty acids. In the rumen, bacterial lipases rapidly break these down and the resulting free unsaturated fatty acids are extensively biohydrogenated, with roughly 90% of linoleic and linolenic acid converted to stearic acid.
Because of this, almost no long-chain fatty acid is absorbed directly from the rumen, omasum or abomasum; the altered free fatty acids pass into the small intestine attached to particulate matter before being absorbed much as in non-ruminants. The paper notes a technical detail here: the amphiphile carrying fat through the gut wall is lysophosphatidyl choline in ruminants rather than the monoacylglyceride used in other species.
Annison also flags a practical limit: dietary fat above about 6-7% can depress cellulose digestion, shift the acetate-to-propionate ratio and reduce methane output, but he cautions that most published studies only report the fat added on top of a basal diet that itself may already contain 2.3% fat, so the true constraints on total dietary fat are not well pinned down.

Protecting fat from the rumen to change meat composition#
Because biohydrogenation erases most of the unsaturation in dietary fat before it reaches the animal, altering the fatty acid make-up of adipose tissue or milk fat requires protecting the fat from rumen bacteria. The original method, developed by Scott and colleagues, coated fat emulsified with sodium caseinate and treated with formaldehyde, allowing it to pass through the rumen intact and still be digested normally in the small intestine.
Feeding protected vegetable oil rich in polyunsaturated fatty acids could sharply change adipose composition: protected safflower oil fed for eight weeks raised the linoleic acid content of bovine subcutaneous fat from about 2% to 25%. A newer approach treats whole oilseeds, after dehulling, with formaldehyde in slurry form, protecting both the protein and the lipid in the seed.
Feedlot trials with canola seed and sunflower meal processed this way improved feed conversion by about 10% and lifted dressing percentage, although the shift in adipose fatty acid composition was less pronounced than with protected oils alone. The author points out that this method also lets producers adjust the protein-to-energy ratio of feedlot rations for better conversion efficiency, a double benefit beyond the fat changes themselves.

Breeding for late maturity: the most reliable lever#
Protein and fat are laid down together in young growing animals, but the paper describes how, beyond a certain body weight, protein accretion levels off while fat gain becomes a large and steady share of further weight gain. Early-maturing animals reach this fattening phase at lighter weights than late-maturing, larger-framed animals.
Because of this pattern, selecting and breeding large, late-maturing animals and slaughtering them at a comparable physiological age, before the fattening phase accelerates, is described in the paper as the most successful strategy so far for producing leaner carcasses. Feed restriction also produces leaner animals, but the paper notes it lengthens the time to market weight, which raises costs under intensive systems, while in Australia's extensive beef operations, limited feed quality in dry seasons already extends time to market without the same deliberate intent.
This conclusion rests on observed growth patterns rather than a single controlled comparison, and the paper is explicit that the underlying biology, why different depots develop asynchronously, for instance, remains unexplained. We would treat the late-maturity strategy as a well-supported general principle rather than a precise formula, since the review itself stops short of quantifying how much leaner late-maturing animals are at any given slaughter weight. The paper's framing of growth and protein accretion connects closely with another review from the same author, on factors affecting protein deposition in ruminants.
Hormones, agonists and the push toward immunological tools#
Intact males grow faster, deposit more protein and carry less fat than castrated or female animals, and the paper describes anabolic steroids, androgenic and oestrogenic, as working by redirecting nutrients from fat toward muscle, partly by boosting growth hormone and insulin secretion. Around 45% of eligible Australian cattle were, at the time, treated with anabolic steroids or growth promotants of similar activity, administered mainly through ear implants to limit residues.
Trenbolone acetate, marketed in Australia combined with oestradiol under the name Revalor, was shown to work mainly by reducing protein breakdown more than protein synthesis, with an added benefit of roughly 10% lower metabolic rate, useful when energy intake is limited, such as in drought. Growth hormone (somatotropin) and synthetic beta-adrenergic agonists such as clenbuterol, cimaterol and ractopamine both reduced fat deposition by increasing lipolysis and suppressing lipogenesis, with agonists cutting fat deposition by about 20% in the production data Annison cites from Bergen and Merkel. Neither growth hormone nor these agonists, however, had been cleared for livestock use in the United States, Europe or Australia by the time of writing.
Immunological approaches are presented as a promising alternative. Blocking somatostatin by immunisation had raised growth hormone release successfully in one non-improved sheep breed, though with less success in commercial breeds. More strikingly, antibodies raised in sheep against rat adipocytes, when injected into rats, cut body fat by up to 50% for six months, while also lifting appetite, growth rate and feed conversion efficiency by about 15%. Annison suggests immunological methods might gain public acceptance more readily than hormone treatments, since they could be seen as akin to vaccination rather than drug administration, though this is offered as a judgement about likely public perception rather than a demonstrated outcome in meat animals.
Sources and further reading#
- Trove library search: find a library that holds the paper
- Meat & Livestock Australia: red meat industry research and marketing body
- Sheep Genetics (LAMBPLAN and MERINOSELECT): which runs LAMBPLAN and MERINOSELECT
- BREEDPLAN genetic evaluation: genetic evaluation system for Australian beef cattle
Questions#
Why do ruminants build fat from acetate instead of glucose?
The paper explains that ruminant tissues have low activity in the enzyme pathways that would normally convert glucose-derived carbon into the acetyl CoA used for fat synthesis, and reduced glycolytic enzyme activity further limits glucose use. Acetate produced during rumen digestion fills this role instead, supplying both carbon and, through related pathways, the reducing power needed for fatty acid production.
Can feeding change the fatty acid composition of beef or lamb fat?
Only if the fat is protected from rumen bacteria, since normal dietary fat is extensively biohydrogenated in the rumen. The paper describes formaldehyde-treated fat or whole oilseed products that survive the rumen intact; protected safflower oil, for example, raised linoleic acid in bovine subcutaneous fat from about 2% to 25% after eight weeks of feeding.
Why were growth hormone and beta-agonists not simply used if they worked so well?
The paper reports that despite proven production benefits, including fat reductions of about 20% with beta-agonists, and no evidence of harm to treated animals or consumers, regulatory authorities in the United States, Europe and Australia had not approved growth hormone or synthetic beta-adrenergic agonists for livestock production at the time of writing.
Is breeding for late-maturing animals still the main way to manage carcase fat?
The paper describes this breeding and selection strategy as the most successful approach available at the time, since large, late-maturing animals reach the fat-accumulating phase of growth later and so can be slaughtered leaner than early-maturing types at a similar market weight. It remains a general growth-pattern principle in the review rather than a precisely quantified outcome.
Written by the Livestock Library team from the published paper by E.F. Annison (1993), and released on 3 October 2026. It is our account of the research in our own words, not the paper itself. For anything you plan to act on, read the original.
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