Obesity is the most prevalent nutritional disorder in cats (Felis catus; Hoenig et al., 2011). High carbohydrate diets, prescribed for weight loss, may contribute to adiposity (Thiess et al., 2004). The effects of a high fat (HF; 30% fat, 10% carbohydrate), high carbohydrate (HC; 10% fat, 46% carbohydrate) and a moderate diet (15% fat, 30% carbohydrate) supplemented with a calorie restriction mimetic (mannoheptulose (MH); 8 mg/kg BW), fed to energy requirements, on feline metabolism and behaviour were investigated (n=20; 4 ± 2.5 kg). An 11 week acclimation procedure was designed to adapt cats to 24-hr restriction within a chamber used for indirect calorimetry. Stress indicative behaviour (Kessler and Turner, 1997) declined with repreated exposure to increasing lengths of restriction within chambers and on week 11 stress levels were low and consistent (P<0.05). Neither the HF nor HC diet impacted body weight (p>0.05); however, HF feeding caused an increase in body fat (0.75 kg (baseline) vs. 1 kg (86d)) after long-term feeding. Energy expenditure (EE) was not impacted by dietary fat/carbohydrate. Respiratory quotients (RQ) increased and decreased with exposure to the HC (fasted= 0.80 ± 0.008; fed= 0.87 ± 0.008), HF (fasted= 0.76 ± 0.008; fed= 0.78 ± 0.008) diet, respectively. Glucose to insulin (G:I) ratio increased with HF feeding; indicating improved insulin sensitivity. Physical activity, measured using accelerometers, declined with HF (-1.6 counts/hr) and HC (-2.8 counts/hr) feeding from baseline. T-maze performance decreased and increased with HF (-0.85 score/10) and HC (0.85 score/10) feeding from baseline (p<0.05). MH did not impact body weight or composition (p>0.05). Area under the curve for EE increased during the 15-22 hour post feeding with MH treatment (2370.3 (-MH) vs. 3292.0 (+MH) ± 0.0002). RQ and G:I were not impacted by MH (p>0.05). MH increased play motivation, measured using obstruction tests (p<0.05). Diets high in carbohydrate are not ideal for weight loss since they negatively impact insulin sensitivity and voluntary EE. Diets promoting elevated EE, activity and normal glucose/insulin profiles are ideal for weight control and MH offers a unique opportunity for use in weight loss regimes. / This work was funded by Procter and Gamble Co.

No description available.

It is becoming increasingly evident that the development of atherosclerotic coronary heart disease (CHD) can largely be regulated by lifestyle and dietary choices. The type of fatty acids regularly consumed may promote or prevent atherogenesis. Flaxseed, the richest plant source of the omega-3 fatty acid alpha-linolenic acid (ALA) is thought to protect against atherosclerotic disease. However, the mechanism(s) by which flaxseed exerts these anti-atherogenic effects requires further investigation. Alternatively, there are dietary fatty acids that are thought to induce significant deleterious effects upon our cardiovascular health. Epidemiological evidence associates dietary trans fatty acids (TFAs) with atherosclerotic CHD. This evidence has largely focused on the main source of TFAs in the North American diet, industrially hydrogenated vegetable shortening (iTFAs). It is assumed that TFAs stimulate atherosclerosis but the only studies to date have shown no effect of TFAs on atherosclerosis. Even less is known of the impact of naturally occurring TFAs from dairy and meat products of ruminant animals (rTFAs) on atherosclerotic disease. We investigated the effects of flaxseed supplementation on atherosclerosis and vascular function in two animal models, the hypercholesterolemic rabbit and the cholesterol fed, low density lipoprotein receptor (LDLr-/-) deficient mouse. New Zealand White rabbits and LDLr-/- mice were fed a diet containing flaxseed in the absence or presence of dietary cholesterol for a period of 6 to 24 weeks. We found that dietary flaxseed inhibits the atherogenic effects of a high cholesterol diet in both animal models. The anti-atherogenic effect was achieved in the mouse model through a capacity to lower circulating cholesterol levels and at a cellular level by inhibiting cell proliferation and inflammation. This reduction is also associated with an improved vascular relaxation response as demonstrated in the rabbit model. We also investigated the effects of consuming TFAs from two sources, industrially hydrogenated iTFAs rich in elaidic TFA (C18:1t-9) or naturally-occurring ruminant rTFAs rich in vaccenic TFA (C18:1t-11), on atherosclerotic development in the LDLr-/- mouse in the presence or absence of elevated dietary cholesterol. Our results demonstrate that consuming iTFAs dose dependently initiates atherosclerotic development but not beyond the effects of dietary cholesterol alone. However, consuming rTFAs rich in vaccenic acid protects against hyperlipidemia and atherosclerosis in the presence or absence of dietary cholesterol. The effects of combining dietary flaxseed and iTFAs in the diet were also examined in this model. Adding whole ground flaxseed or flaxseed oil (ALA) to diets containing low and high doses of iTFAs completely prevented atherosclerotic development in the absence of dietary cholesterol. Flaxseed was also able to partially prevent atherosclerosis caused by iTFAs and cholesterol. Our results suggest that the omega-3 ALA fatty acid rich content of flaxseed is mainly responsible for the anti-atherogenic effects of flaxseed. Our results highlight potential mechanisms for the beneficial effects of dietary flaxseed and the mixed effects of TFAs on cardiovascular health and underscore the need for further basic and clinical investigations.

Anticipatory satiety is the ability to reduce meal size when the diet at that meal is consistently followed by a short time interval to the next access to food. This prediction of intake is learnt, i.e. based on the association of a food's sensory characteristics with some consequence(s) of ingesting it. / Two pilot studies were conducted using male Sprague-Dawley rats in which (1) the ability of food texture to cue fasting duration was indicated by evidence of anticipatory satiety in the low-fat powder-long/paste-short group and in the high-fat paste-long/powder-short group and (2) the pattern of anticipatory satiety was seen only in the low-fat granules-long/powder-short group. / In the main experiment (n = 9), anticipatory satiety was reached twice in the highfat powder-long/pellet-short group on days 16--23 (p &le; 0.1) and once in the low-fat pellet-long group/powder-short on days 20--23 (p &le; 0.1). The acquisition of texture-cued fasting-anticipatory satiety seems to depend upon high-energy density of the diet and the utilisation of textures which make it easier for the rats to eat.

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Despite similar rates of energy expenditure during training, competitive swimmers have been shown to store significantly greater amounts of body fat than competitive runners. In an attempt to explain these discrepancies, male collegiate swimmers (n=8) and runners (n=8) were monitored during 45 min of swimming and running, respectively (75% V02 max), and during two hours of recovery. In addition, a group of male competitive triathletes (n=6) were similarly monitored during and after both swimming and running exercise.Blood samples were obtained after 15 min rest prior to exercise and at 0, 15, 30, 60 and 120 min of recovery and were analyzed for glucose, lactate, glycerol, free fatty acids, insulin, glucagons, norepinephrine (NE) and epinephrine (E). Respiratory gases were collected at 15 min intervals during exercise and at 15, 30, 45, 60, 90 and 120 min of recovery. Heart rate and mean body temperature were recorded at 10 min intervals throughout recovery. There were no differences in post-exercise oxygen consumption or heart rate while the RER suggested increased fat oxidation after exercise for the swimmers and the swimming triathletes. The mean body temperature and mean skin temperatures were significantly lower throughout 120 min of recovery for the swimmers compared to the runners. The triathletes demonstrated a similar tendency but these differences were not significant. The serum glucose levels were significantly greater (P<0.05) immediately post-exercise for the runners compared to the swimmers (6.71 +0.29 and 4.97 +0.19 mmol•1-1, respectively). Blood glucose values were also significantly greater immediately post-run for the triathletes (6.40 +0.26 and 4.87 ±0.18 mmol-l-1 for running and swimming, respectively). Blood glucose values remained elevated for runners and the running triathletes up to 30 min of recovery. Free fatty acids were similar after the run and the swim, but glycerols were increased immediately after running in the runners (P<0.05) and the triathletes (P<0.05). Differences in blood glucose levels or fat release were not explained by differences in NE, E or cortisol. The glucagon-to-insulin (G:I) ratio was significantly increased after exercise in the swimmers and the swimming triathletes. This, combined with a reduced RER after the swimming trials, suggests that the reduced glucose levels were due to reduced hepatic glycogen stores. The results of this study suggest that there were differences in substrate utilization during running and swimming exercise of the same intensity. These differences were not explained by NE, E or cortisol; however, the increased G:T ratio suggests increased carbohydrate use during exercise in the swimmers. Finally, body fat differences between runners and swimmers were not explained by differences in post-exercise energy expenditure or fat oxidation.

Dietary fatty acids are considered promoters of murine and human mammary tumors. The mechanism responsible is not known. Mammary adenocarcinomas in mice originate from preneoplastic cells (hyperplastic alveolar nodules (HAN)) which are derived from normal mammary epithelial cells. Diets rich in linoleic acid (18:2) have been associated with increased incidence of HAN and promotion of tumor growth. Diets rich in stearic acid (18:0) have been associated with decreased incidence of HAN and increased latency period for mammary tumor formation in mice.The effects of dietary 18:0 and 18:2 stages of murine mammary tumorigenesis were examined. The purpose of this study was to determine the effects of these dietary fatty acids on HAN production, mammary gland development, and fatty acid composition of mammary epithelial cells and adipocytes.Spontaneous mammary tumor producing strain A/ST mice were fed a high fat (15%) or low fat (5%) diet. High fat stock (ST) diet containing 1.5% 18:2 or a low fat corn oil (CO) diet containing 3% 18:2 were fed. Animals were sacrificed at 6 or 10 months of age. HAN, ductile and alveolar development were histologically determined in the left inguinal mammary gland. The contralateral gland was on the early diets rich in 18:2 (SF) or 18:0 (SA) were fed. A low*fat enzymatically dissociated and fatty acid compositions of adipocyte and epithelial cells were determined by GLC. Fatty acid profiles were examined for correlation to histologic findings.SA-fed mice had fewer HAN and less well developed mammary alveoli than the other dietary groups which exhibited moderate (ST) or high (CO, SF) HAN incidence. SF-fed mice had the earliest onset of any dietary group. CO-fed mice had later onset of HAN as compared to SF-fed mice but the HAN incidence was similarly high in both groups at 10 months of age.SA-fed mice were protected from development of expected numbers of HAN as compared to ST-fed mice. The reduction in HAN risk in this group was associated with reduced mammary alveolar development. Groups with high risk of HAN (SF and CO) exhibited increased amounts of 18:2 in their mammary epithelial cells and adipocytes. / Department of Biology

It is becoming increasingly evident that the development of atherosclerotic coronary heart disease (CHD) can largely be regulated by lifestyle and dietary choices. The type of fatty acids regularly consumed may promote or prevent atherogenesis. Flaxseed, the richest plant source of the omega-3 fatty acid alpha-linolenic acid (ALA) is thought to protect against atherosclerotic disease. However, the mechanism(s) by which flaxseed exerts these anti-atherogenic effects requires further investigation. Alternatively, there are dietary fatty acids that are thought to induce significant deleterious effects upon our cardiovascular health. Epidemiological evidence associates dietary trans fatty acids (TFAs) with atherosclerotic CHD. This evidence has largely focused on the main source of TFAs in the North American diet, industrially hydrogenated vegetable shortening (iTFAs). It is assumed that TFAs stimulate atherosclerosis but the only studies to date have shown no effect of TFAs on atherosclerosis. Even less is known of the impact of naturally occurring TFAs from dairy and meat products of ruminant animals (rTFAs) on atherosclerotic disease. We investigated the effects of flaxseed supplementation on atherosclerosis and vascular function in two animal models, the hypercholesterolemic rabbit and the cholesterol fed, low density lipoprotein receptor (LDLr-/-) deficient mouse. New Zealand White rabbits and LDLr-/- mice were fed a diet containing flaxseed in the absence or presence of dietary cholesterol for a period of 6 to 24 weeks. We found that dietary flaxseed inhibits the atherogenic effects of a high cholesterol diet in both animal models. The anti-atherogenic effect was achieved in the mouse model through a capacity to lower circulating cholesterol levels and at a cellular level by inhibiting cell proliferation and inflammation. This reduction is also associated with an improved vascular relaxation response as demonstrated in the rabbit model. We also investigated the effects of consuming TFAs from two sources, industrially hydrogenated iTFAs rich in elaidic TFA (C18:1t-9) or naturally-occurring ruminant rTFAs rich in vaccenic TFA (C18:1t-11), on atherosclerotic development in the LDLr-/- mouse in the presence or absence of elevated dietary cholesterol. Our results demonstrate that consuming iTFAs dose dependently initiates atherosclerotic development but not beyond the effects of dietary cholesterol alone. However, consuming rTFAs rich in vaccenic acid protects against hyperlipidemia and atherosclerosis in the presence or absence of dietary cholesterol. The effects of combining dietary flaxseed and iTFAs in the diet were also examined in this model. Adding whole ground flaxseed or flaxseed oil (ALA) to diets containing low and high doses of iTFAs completely prevented atherosclerotic development in the absence of dietary cholesterol. Flaxseed was also able to partially prevent atherosclerosis caused by iTFAs and cholesterol. Our results suggest that the omega-3 ALA fatty acid rich content of flaxseed is mainly responsible for the anti-atherogenic effects of flaxseed. Our results highlight potential mechanisms for the beneficial effects of dietary flaxseed and the mixed effects of TFAs on cardiovascular health and underscore the need for further basic and clinical investigations.

No description available.