Two trials were conducted to study the effect of feeding a protected-fat supplement on reproduction. In the first trial eight ovariectomized brangus cows were used to study the effect of feeding a protected-fat supplement on LH release after GnRH injection. The cows were equally divided at random into two groups (control and treatment), placed in individual pens, and fed a ration supplying 4.0 kg of TDN per head daily. Cows in the treatment group received a .68 kg of protected fat daily for the entire experimental period (30 days). On the last day of the experiment an indwelling jugular catheter was inserted into the cows and blood samples were taken every ten minutes for a period of 5 hours. After the sixth sample was taken, 200 (mu)g of GnRH were injected intramuscularly to induce LH release. The samples taken before the GnRH was injected were used to establish basal LH levels. LH levels were analyzed by using the double antibody radioimmunoassay technique. Average weight of the cows at the start of the trial for the control and treatment group were 491 and 457 kg respectively. Cows in the control group lost weight (-8 kg) during the experimental period, whereas those in the treatment group gained 33 kg. The highest LH peak value was 12 ng/ml for the controls and 43 ng/ml for the treated cows. Mean LH values were 4.9 ng/ml for the control group and 43 ng/ml for the treatment group. In the second experiment twenty multiparous four-year-old pregnant brangus cows are used to determine the effect of a protected fat diet on postpartum pituitary response to GnRH. As cows calved they were randomly assigned to either the control or treatment group. The treatment consisted of adding .68 kg of protected fat to the ration. The diet for both groups was designed to supply approximately 4.4 kg of TDN daily per animal. This was about 80% of the NRC requirement. On day 7 postpartum an indwelling catheter was inserted into the jugular vein. Blood samples were taken for 5 hours every ten minutes. After the sixth sample was taken 200 (mu)g of GnRH were injected intramuscularly to induce LH release. The pre-GnRH injection period was used to establish basal LH levels. Luteinizing hormone levels were analyzed using the radioimmunoassay double antibody technique. The latter part of this experiment was designed to assess the effect of a protected fat diet on postpartum estrus activity. Estrus was also checked by daily visual observation. Average weight of the cows at the start of the experiment was 514 and 474 kg for the control and the treatment group respectively. By the end of the trial (75th day) cows in the control group lost 35 kg, and those in the treatment group lost 22 kg. Average daily gain of calves whose mothers were on treatment or control did not differ. Mean LH levels were 18 and 13 ng/ml for the treatment and control cows respectively. This difference was not statistically significant due to a large mean standard error. Fifty percent of the cows receiving the protected fat supplement had shown standing estrus by day 45 postpartum vs 20% for the control group. By day 15 pospartum 60% of the cows in the treatment group had shown signs of postpartum estrus activity vs only 10% for the control group. By day 45 postpartum all the cows receiving the protected fat supplement had shown signs of estrus activity vs only 50% for the control.

No description available.

The clearance of circulating glucose and long-chain fatty acids (FA) into skeletal muscle involves the translocation of glucose transporter GLUT4, fatty acid translocase (FAT/CD36), plasma membrane associated fatty acid binding protein (FABPpm) and fatty acid transport protein (FATP) 1 and 4 to the plasma membrane (PM). FAT/CD36 also appears to participate in the regulation of mitochondrial FA oxidation. Metabolic challenges are known to increase FA transport and/or oxidation, but whether this is solely attributable to the translocation of FAT/CD36 to the sarcolemma and/or mitochondria is unknown. Moreover, the signaling and trafficking pathways involved in the translocation of FA transporters are largely unexplored. In this thesis it was found that FA transport was markedly increased following insulin (+2.9-fold) or contraction (+1.7-fold) stimulation of skeletal muscle, along with the PM contents of FAT/CD36 (+78%, +55%,), FABPpm (+61%, +62%), FATP1 (+84%, +61%) and FATP4 (+60%, +66%) (p<0.05). Upon combining the two stimuli, only the translocation of FAT/CD36 (+179%) and FATP1 (+125%) to the PM was additive, suggesting that these transporters may reside in distinct insulin-sensitive and contraction-sensitive intracellular compartments. The translocation of FA transporters may involve the insulin-signaling protein Akt2. It was found that insulin-stimulated FA transport and PM translocation of FA transporters was essentially prevented in Akt2 knockout mice. Following contraction, FA transport was also markedly blunted, along with an impaired translocation of both FAT/CD36 and FATP1, but not FABPpm or FATP4. FA oxidation and mitochondrial FAT/CD36 appearance were also inhibited following muscle contraction in knockout mice (p<0.05). Whether the GLUT4 trafficking protein Munc18c is important for the vesicular re-distribution of FA transporters to the PM or mitochondria was also investigated. FA uptake was comparably increased 1.4 fold with insulin and contraction in both wildtype and heterozygous Munc18c-/+ mice, as were PM FA transporters FAT/CD36 (+82%, +84%), FABPpm (+39%, +43%), FATP1 (+40%, +38%) and FATP4 (+33%, +32%) (p<0.05). Contraction-stimulated mitochondrial FA oxidation was also increased similarly in wildtype (+39%) and Munc18c-/+ mice (+33%). These studies demonstrate that a number of FA transporters are involved in upregulating skeletal muscle FA transport, although their signaling and trafficking pathways may differ from that of GLUT4.

I examined the influence of cyclic feeding regime on fillet yield and quality and their genetic architecture in rainbow trout (Oncorhynchus mykiss). Two lots of half-sib families produced in September and December were exposed to periods of reduced ration followed by increased ration. Fish fed cyclically reduced rations weighed less and had smaller fillets and body proportions relative to controls. They also had less estimated muscle and visceral lipid but also more proportional visceral mass. Lots and families within lots differed significantly for the majority of traits. Genotypic analysis with 23 microsatellite markers spanning 19 linkage groups detected QTL for all traits over multiple linkage groups that were not necessarily consistent between feeding regime and parental lot. Linkage groups RT-9 and 29 had the largest QTL effects for fillet composition traits and overall body size across the greatest number of parents sampled.

Excessive abdominal obesity, coupled with a decline in muscle mass and physical function that is exacerbated by sedentary living, contributes substantively to the disease and disability common to our aging population. The Senior Study, a randomized controlled trial designed to investigate the health benefits associated with performing resistance exercise (RE), aerobic exercise (AE), or a combination of both exercise modalities (RAE) for six months in the absence of caloric restriction, was conducted on otherwise healthy but abdominally obese, sedentary men (n=57) and women (n=79) between the ages of 60 and 80. The purpose of the first manuscript (Chapter 3) was to compare the effects of exercise modality on visceral obesity and insulin resistance in the Senior Study. All exercise groups significantly reduced total abdominal and visceral fat (P<0.05) and waist circumference (P<0.001), which measure explained 30% of the variance in total abdominal fat changes (P<0.001). AE and RAE improved insulin sensitivity (P<0.05), but the RE group did not (P>0.1). The greatest insulin sensitivity increase was observed within the RAE group (48% increase, P<0.001). The purpose of the second manuscript (Chapter 4) was to evaluate the effects of exercise modality on cardiorespiratory and functional fitness in the Senior Study. AE and RAE increased cardiorespiratory fitness (P<0.001), whereas RE did not (P>0.1). All exercise groups improved functional fitness performance (P<0.001), but age- and sex-specific percentile ranking improvement within RAE was greater than AE (P<0.01). RE and RAE significantly increased skeletal muscle (P<0.01), predominantly in the upper body, while AE did not (P=1.0). AE and RAE reduced total fat (P<0.001). Both fat loss and muscle gain were independent predictors of improvements in functional fitness (P<0.05). The findings from these studies demonstrate conclusively that a combined resistance and aerobic exercise program without caloric restriction is an optimal strategy for the therapeutic reduction of health risk in abdominally obese men and women. While each exercise modality offers distinct benefits and remains a viable option for needs-based exercise prescription, the combination was associated with the greater simultaneous improvements to body composition, insulin resistance, and cardiorespiratory and functional fitness than either resistance or aerobic exercise alone. / Thesis (Ph.D, Kinesiology & Health Studies) -- Queen's University, 2007-09-13 13:21:31.772

Dehulled black beans were micronized at 90⁰C, 100⁰C, 110⁰C, 120⁰C, 130⁰C and 140⁰C; milled to flour and tested for lipoxygenase activity. Non micronized black bean flour was higher in lipoxygenase activity than flours at ≥120ºC (p=≤0.05). Micronized (100⁰C, 110⁰C, 120⁰C) and non micronized black bean flour was added to low fat beef burgers (6%). C18:3 was significantly higher in the black bean flour samples (raw and cooked). Whole wheat flour had the highest amount of C18:2 in all samples (p= ≤0.05). The all beef control was significantly higher in Newton value, drip loss, cook loss and percent shrinkage compared to burgers with binders (p= ≤0.05). Ninety-three participants participated in an consumer sensory panel. Results showed higher acceptability of micronized burgers compared to all beef or whole wheat flour controls. This study demonstrated incorporation of black bean flour into low fat beef burgers can improve their physical, chemical and sensory properties.

BACKGROUND: Diaclyglycerol (DAG) oil has the potential as an effective weight control agent as well as an agent to modify overweight related complications. OBJECTIVE: We aim to examine the efficacy of DAG oil (Enova oilTM) on regulating energy expenditure (EE), fat oxidation, body composition, lipid profiles and hepatic lipogenesis in comparison with conventional oils. DESIGN: Twenty-six overweight hypertriglyceridemic women consumed DAG or control oil for 28 days separated by a 4-week washout period using a randomized crossover design. Forty grams of either DAG or control oil were consumed daily by each study subject. RESULTS: DAG oil consumption for a period of 4-week does not alter total EE, fat oxidation, lean mass, fasting lipid profile or fatty acids synthesis rate, but effectively reduces (p<0.05) body weight and adiposity. CONCLUSION: DAG oil maybe an useful agent in the battle against obesity. However, its body weight/composition control effects are not from increasing of lean mass, or postprandial EE and fat oxidation. The consumption of DAG oil for a period of 4-week does not necessarily modify fasting lipid profiles or hepatic lipogenesis to reduce risk of coronary heart diseases in overweight hypertriglyceridemic subjects.

Processes that regulate site of fat deposition in beef cattle are poorly understood. For the producer to procure the greatest profit, it is ideal to maximize intramuscular fat. Furthermore, to understand the physiological mechanisms affecting fat depots, it is necessary to evaluate hormones involved in growth regulation. Using a 2 x 2 factorial design of treatments, four experiments were conducted to examine two adipogenic compounds, chlortetracycline and dexamethasone. Synovex-S® and Revalor-S® were used to investigate potential interactions between growth implants and adipogenic compound. Growth performance, carcass quality, organ and fat mass and plasma hormone concentrations were measured in these studies. In Exp. 1, 24 steers received either 0 or 350mg chlortetracycline/d, with or without Synovex-S®. On d 30, 56 and 106, steers received a bolus injection of 1 ug/kg BW thyrotropin-releasing hormone and 0.1 ug/kg BW GH-releasing hormone and serial blood samples were collected. Synovex-S® increased (P ≤ 0.009) rate and efficiency of gain and decreased (P = 0.05) time to peak for GH concentrations. Chlortetracycline attenuated (P ≤ 0.05) the effects of implant on triiodothyronine release, slaughter weight and carcass quality. In Exp. 2, 96 steers received either 0 or 39.6 ppm chlortetracycline/d, with or without Revalor-S®. Implant increased (P < 0.0001) ADG; however, efficiency of gain was greater for implanted steers in the absence of chlortetracycline (interaction, P ≤ 0.03). In Exp. 3, 144 steers received either 0 or 0.09 mg dexamethasone/kg BW on d 0, 28 or 56, with or without Revalor-S®. Average daily gain was lower (P = 0.0003) for implanted steers receiving dexamethasone compared to those receiving no dexamethasone (interaction, P = 0.05). Omental fat mass was greater (P = 0.01) for non-implanted steers receiving dexamethasone compared to no dexamethasone (interaction, P = 0.006). In Exp. 4, 96 steers received either 0 or 0.09 mg dexamethasone/kg BW on d 0, 28, 56 or 84, with or without Revalor-S®. Average daily gain and efficiency of gain were both 13% greater (P ≤ 0.05) with implant. Conversely, DEX lowered ADG by 10% (P = 0.007). There were no effects of treatment on fat mass weights.

Hyperhomocysteinemia, an elevation of blood homocysteine levels, is a metabolic disorder associated with dysfunction of multiple organs. Previous studies have shown that hyperhomocysteinemia is related to fatty liver. However, the underlying mechanism remains speculative. The objective of the present study is to investigate the regulatory mechanism of hepatic inflammatory response and cholesterol metabolism during metabolic disorders. In the present study, hyperhomocysteinemia was induced in Sprague-Dawley rats by feeding a high-methionine diet. The mRNA and protein expression of cyclooxygenase-2 (COX-2), a pro-inflammatory factor, were significantly elevated in the liver of hyperhomocysteinemic rats. An activation of NF-B and a stimulation of oxidative stress were observed in the same liver tissue in which COX-2 was induced. Inhibition of NF-B or oxidative stress effectively abolished hepatic COX-2 expression, inhibited the formation of inflammatory foci, and improved liver function. Activity of HMG-CoA reductase, the rate-limiting enzyme of cholesterol biosynthesis, was markedly elevated in the liver of hyperhomocysteinemic rats, which may contribute to the hepatic lipid accumulation induced by hyperhomocysteinemia. Administration of Berberine (5mg/ kg body weight/ day for 5 days) inhibited HMG-CoA reductase activity via upregulating AMP-activated protein kinase (AMPK)-mediated phosphorylation of HMG-CoA reductase. Berberine treatment reduced hepatic cholesterol content and ameliorated liver function. In addition, the regulatory mechanism of HMG-CoA reductase activation was investigated in C57BL/6 mice fed a high-fat diet. There was a significant increase in hepatic HMG-CoA reductase mRNA and protein expression as well as enzyme activity. The DNA binding activity of sterol regulatory element binding protein (SREBP)-2 (a transcription factor of HMG-CoA reductase) and Sp1 (a transcription factor of SREBP-2) were both increased in the liver of mice fed a high-fat diet. The in vitro study in palmitic acid-treated HepG2 cells further confirmed that inhibition of Sp1 by siRNA transfection abolished palmitic acid-induced SREBP-2 and HMG-CoA reductase mRNA expression. In conclusion, the present study have demonstrated that (1) Hepatic COX-2 expression is induced via oxidative stress mediated NF-B activation during hyperhomocysteinemia; (2) Dietary berberine reduces cholesterol biosynthesis by elevating AMPK-mediated HMG-CoA reductase phosphorylation; (3) HMG-CoA reductase is upregulated by Sp1-mediated SREBP-2 activation in the liver during high-fat diet feeding.

The normal development of adipose tissue lipolysis as measured by glycerol release was studied in epididymal fat pads of Sprague-Dawley rats between 4 and 16 weeks of age and correlated with changes in fat cell size.For each age group studied, 4 weeks, 8 weeks, and 16 weeks of age, basal (no hormone present) and hormone stimulated lipolytic activity were observed for two concentrations of epinephrine were used, maximal (10,00 nM) and minimal (10 nM). Basal levels of glycerol were not linear. There was an increase between 4 and 8 weeks of age followed by a decrease between 8 and 16 weeks of age. The maximal dosage of hormone evoked a large increase in 9lYcerol production between 4 and 8 weeks, which was followed by a decrease between 8 and 16 weeks of age. The minimal dosage of epinephrine, although not significant, showed a decrease in glycerol production from 4 to 16 weeks of age. Fat cell size continued to increase between 4 and 16 weeks. Both fat cell diameter and volumes underwent a linear increase with age. However, the change was not reflected in epinephrine stimulated glycerol release. Therefore, glycerol release is inversely correlated with fat cell size during early development.The results indicate that age influences hormone stimulated lipolysis and is not dependent on cell size. Although the mechanism for the decreased lipolytic response of the isolated adipocytes was not discovered, it is believed that it may be due in part to a reduced number of receptors and to a reduced sensitivity of the cellular enzymatic system underlying lipolysis. / School of Physical Education