Effect of Conjugated Linoleic Acid on Insulin Sensitivity

Mice were fed a mixture of conjugated linoleic acid isomers (CLA) for nine weeks and then underwent an insulin tolerance test. CLA was then removed from the diet and a second insulin tolerance test was conducted following five weeks of recovery. CLA consumption impaired glucose response to insulin. When CLA was removed from the diet, insulin sensitivity of a low heat-loss genetic mouse line returned to normal. However, mice of a high heat-loss line remained insulin resistant for at least 32 days

Effect of Conjugated Linoleic Acid on Insulin Sensitivity

Mice were fed a mixture of conjugated linoleic acid isomers (CLA) for nine weeks and then underwent an insulin tolerance test. CLA was then removed from the diet and a second insulin tolerance test was conducted following five weeks of recovery. CLA consumption impaired glucose response to insulin. When CLA was removed from the diet, insulin sensitivity of a low heat-loss genetic mouse line returned to normal. However, mice of a high heat-loss line remained insulin resistant for at least 32 days

Short communication: Detection of yeast DNA in omasal digesta of dairy cows consuming dried distillers grains and solubles

Purine analysis is widely used to estimate microbial crude protein (MCP) flow, and the method assumes that all purines contained in feed are degraded in the rumen and that purines detected are of microbial origin. The objectives of our experiment were (1) to determine if DNA from yeast (Saccharomyces cerevisiae) contained in dried distillers grains and solubles (DDGS) escapes degradation in the rumen and (2) to estimate the proportion of yeast DNA compared with total bacterial DNA in omasal samples. Two ruminally fistulated Holstein dairy cows averaging 649 kg (SD = 42.0) and 126 d in milk (SD = 28.9) were fed in a crossover design during 2 periods of 21 d each. Treatments were (1) control, a total mixed ration (TMR) not containing DDGS and (2) a DDGS-based diet, a TMR in which DDGS were included at 30% of diet dry matter (DM). On d 20 and 21 at 0400 and 1600 h, omasal digesta samples were collected via a ruminal cannula, and DNA was extracted from each sample in duplicate. The DNA samples were subjected to a realtime PCR assay to detect the presence of DNA from yeast. Forward and reverse primers and a probe were designed to target a DNA segment contained on the second chromosome of Saccharomyces cerevisiae. Realtime PCR amplification curves indicated the presence of yeast DNA in samples from both treatments. Specifically, the estimate of relative abundance of yeast DNA from digesta samples collected from animals consuming the diet containing DDGS was 9.46 ± 0.67/g of DM and was significantly higher than that from animals consuming no DDGS, which was observed to be 0.091 ± 0.67/g of DM. Omasal samples were also analyzed for total bacterial DNA. Primers and a probe were designed from DNA encoding part of the 16S rRNA. When the DDGS-based diet was fed, the relative abundance of total bacterial DNA tended to increase from 610 to 626 ± 3.82/g of DM. Results suggest that yeast DNA is detected in the omasum and this is increased when cows consume DDGS but it does not represent a significant proportion of total microbial DNA in the omasal digesta samples

Short communication: Detection of yeast DNA in omasal digesta of dairy cows consuming dried distillers grains and solubles

Purine analysis is widely used to estimate microbial crude protein (MCP) flow, and the method assumes that all purines contained in feed are degraded in the rumen and that purines detected are of microbial origin. The objectives of our experiment were (1) to determine if DNA from yeast (Saccharomyces cerevisiae) contained in dried distillers grains and solubles (DDGS) escapes degradation in the rumen and (2) to estimate the proportion of yeast DNA compared with total bacterial DNA in omasal samples. Two ruminally fistulated Holstein dairy cows averaging 649 kg (SD = 42.0) and 126 d in milk (SD = 28.9) were fed in a crossover design during 2 periods of 21 d each. Treatments were (1) control, a total mixed ration (TMR) not containing DDGS and (2) a DDGS-based diet, a TMR in which DDGS were included at 30% of diet dry matter (DM). On d 20 and 21 at 0400 and 1600 h, omasal digesta samples were collected via a ruminal cannula, and DNA was extracted from each sample in duplicate. The DNA samples were subjected to a realtime PCR assay to detect the presence of DNA from yeast. Forward and reverse primers and a probe were designed to target a DNA segment contained on the second chromosome of Saccharomyces cerevisiae. Realtime PCR amplification curves indicated the presence of yeast DNA in samples from both treatments. Specifically, the estimate of relative abundance of yeast DNA from digesta samples collected from animals consuming the diet containing DDGS was 9.46 ± 0.67/g of DM and was significantly higher than that from animals consuming no DDGS, which was observed to be 0.091 ± 0.67/g of DM. Omasal samples were also analyzed for total bacterial DNA. Primers and a probe were designed from DNA encoding part of the 16S rRNA. When the DDGS-based diet was fed, the relative abundance of total bacterial DNA tended to increase from 610 to 626 ± 3.82/g of DM. Results suggest that yeast DNA is detected in the omasum and this is increased when cows consume DDGS but it does not represent a significant proportion of total microbial DNA in the omasal digesta samples

Hormonal Influence on Fat Synthesis in Cattle

The ability of adenosine, insulin and human acylation-stimulating protein to modify fat synthesis was determined using cultures of fat tissue from steers. Adenosine did not influence fat synthesis. However, acylation stimulating protein and insulin promoted fat synthesis. These observations, coupled with knowledge of how fat synthesis is regulated in other species, justify investigation of whether cattle synthesize acylation-stimulating protein, and how this synthesis is regulated. An understanding of how acylation-stimulating protein production and action is regulated should expose potential places for intervention to manipulate fat synthesis in cattle

Acylation Stimulating Protein: A Potential Regulator of Fat Synthesis

The long term goal of this project is to understand the molecular mechanisms controlling fat synthesis. These experiments indicate that acylation stimulating protein (ASP) can stimulate the incorporation of fatty acids into lipid in cultured adipose tissue. This finding justifies a future effort to determine if manipulation of ASP can modify fat deposition

Conjugated Linoleic Acid Metabolism and Body Fat Loss in Mice

Mice were fed conjugated linoleic acid (CLA) with or without fish oil or aspirin, which deplete tissue arachidonic acid and block arachidonic acid metabolism, respectively. Mice fed fish oil did not lose body fat when supplemented with CLA but mice fed soy oil did. Aspirin did not alter CLA-induced body fat loss. CLA may be metabolized to an isomer of arachidonic acid to induce a loss of body fat. However, this body fat loss is apparently not mediated via alteration of prostaglandin synthesis. Understanding the regulation of body fat by CLA may offer insight into the mechanisms of body fat regulation in cattle

Effect of Conjugated Linoleic Acid on Cell Death in Adipose Tissue

Mice fed conjugated linoleic acid (CLA) lose body fat. This loss of body fat is accompanied by an increases in DNA fragmentation, indicative of apoptosis or programmed cell death. Adipose apoptosis was observed in mice fed the trans-10, cis-12 isomer or a mixture of isomers but not the cis-9,trans-11 isomer. The trans-10,cis-12 isomer also induced DNA fragmentation in preadipocytes in vitro, but not mature adipocytes. The cis-9,trans-11 CLA isomer, the predominant isomer in ruminant-derived products, was reported to induce apoptosis of cancer cells. Determining the mechanism of action of CLA will improve our understanding of body fat regulation

Influence on Body Fat of Linoleic Acid Isomers

In two studies mice were fed diets containing either a mixture of, or individual conjugated linoleic acid (CLA) isomers in the presence or absence of essential fatty acids. Mice fed the C18:2 Δ10,12 CLA isomer lost as much body fat as those fed a mixture of isomers. This effect was not caused by the C18:2 Δ9,11 isomer (predominant in beef) or by restricted feed intake. The loss was much greater in mice consuming an essential fatty acid deficient diet versus a control diet. This supports our hypothesis that for CLA to deplete body fat, it must first be metabolized in a manner similar to linoleic acid. Furthermore, we suggest that the loss of body fat may be mediated by metabolism of CLA to an isomer of arachidonic acid

Influence of Linoleic Acid Isomers on Body Fat

In two studies, mice were fed diets containing either individual conjugated linoleic acid (CLA) isomers or a mixture of isomers in the presence or absence of dietary essential fatty acids. Mice fed the C18:2 Δ10,12 CLA isomer lost as much body fat as mice fed a mixture of isomers. This effect was not observed when the mice were fed the C18:2 Δ9,11 isomer or when feed intake was restricted. The loss of body fat was much greater in mice consuming an essential fatty acid deficient diet versus a control diet. This supports our hypothesis that for CLA to deplete body fat, it must first be metabolized in a manner similar to linoleic acid. Furthermore, we suggest that the loss of body fat may be mediated by metabolism of CLA to an isomer of arachidonic acid. Understanding the mechanism by which CLA causes body fat loss, in pigs as well as mice, will allow for greater regulation of body fat content