Long-term, high protein diets at 35% of energy may have implications in bone biology. The objective of this study was to comprehensively examine whether a high mixed protein diet at the 35% energy level can be deemed safe with respect to long-term bone health. Eighty female Sprague-Dawley rats were randomized to receive 4, 8, 12, or 17 months of a control (15% of energy as protein) or the high protein diet (35% of energy). Statistical analyses of biochemical, biomechanical, morphological, microarchitectural, and densitometric examinations using a 2-way factorial ANOVA with interaction revealed that elevated protein consumption had no negative consequences to bone health. High protein fed rats had increased lean body mass and decreased body weight and body fat. Thus preliminary results suggest that protein consumption at 35% of energy has a positive effect on body weight and does not hinder the mechanical abilities of bone.

Urotensin-II (U-II) and its receptor UT are upregulated in the pathological setting of various cardiovascular diseases including atherosclerosis. However, their exact role in atherosclerosis remains to be determined. In the present study, we hypothesized that selective overexpression of UT in an SMC-specific fashion would increase atherosclerotic lesion formation in a hypercholesterolemic mouse model. The objectives were to demonstrate the role of UT in this mouse model of atherosclerosis, and to elucidate some of the mechanism involved in the process. We used four strains of mice; wildtype (WT), UT+ (a transgenic strain expressing human UT driven by the alpha-SM22 promoter), ApoE knockout (ko), and UT+/ApoE ko. All animals were fed a high-fat diet for 12 weeks. Western blot analysis revealed a significant increase in UT expression in UT+ and ApoE ko mice (P<0.05). Serum cholesterol and triglyceride levels were significantly increased in ApoE ko and in UT+/ApoE ko but not in UT + mice when compared to wild type mice (P<0.0001). Analysis of aortas showed a significant increase in atherosclerotic lesion in the UT +, ApoE ko and UT+/ApoE ko compared to WT mice (P<0.05). Oral administration of the UT receptor antagonist SB-657510A for 10 weeks in a group of ApoE ko mice fed a high fat diet resulted in a significant reduction of lesion (P<0.001). Immunohistochemistry revealed the presence of strong expression of UT and U-II proteins in the atheroma of UT+, ApoE ko and UT+/ApoE ko mice, particularly in foam cells. SB-657510A also significantly reduced ACAT-1 protein expression in the atherosclerotic lesion of ApoE ko mice (P<0.05). The present findings suggest that the use of UT receptor antagonists may reduce lesion formation through reduced foam cell formation and lipid uptake, demonstrating an important role for UT in the pathogenesis of atherosclerosis.

The ability of animals to contend with unpredictable seasonal shifts in quality and quantity of prey has implications for the conservation of wildlife. Steller sea lions(Eumetopias jubatus) were subjected to different quantities and qualities of food to determine what physiological and endocrine responses would occur and whether they differed between season (summer and winter) or diet (high-lipid Pacific herring Clupeapallasi vs. low-lipid Walleye Pollock Theragra chalcogramma). Eight females were divided among two groups. One (Group H) were fed herring for 28 days (baseline), then received a reduced caloric intake for a subsequent 28 days (restriction) to induce a 15%loss of body mass. The second (Group P) were also fed herring during the baseline followed by a reduced isocaloric diet of pollock during the restriction. Both groups subsequently returned to their baseline intake of herring for a 28-day controlled re-feeding. The two groups of sea lions lost identical mass during restrictions independent of species eaten, but did differ in the type of internal energy reserve (protein vs. lipids) they predominantly used. Group H lost significantly more lipids and less lean mass than Group P in both seasons. In summer, Group H also increased activity levels and decreased thermoregulation capacity to optimize energy allocation. No such changes were observed for Group P whose capacity to adjust to the reduced caloric intake seemed to have been blocked by the pollock diet. During winter, the sea lions spared energy allocated to activity (especially Group H) and preserved thermoregulation capacity. Changes in body mass was negatively related to free cortisol and positively related to IGF-1 in winter, but only IGF-1 was related to changes in mass in summer when lean mass regulation seemed more important. Levels of IGF-1 were associated with changes in protein metabolism in both seasons for both groups, but changes in body condition were never explained by the measured metabolites or hormones. The capacity to compensate for mass loss was seasonally dependent with sea lions displaying compensatory growth (by restoring lipid stores) in winter but not in summer. Summer appears to be a more difficult season for sea lions to recover from mild nutritional stress. These physiological findings can be used to refine bioenergetic models needed for the conservation of Steller sea lion populations.

Succinic semialdehyde dehydrogenase (ALDH5A1) deficiency (SSADH-d) is an autosomal recessive, inborn error of gamma-aminobutyric acid (GABA) metabolism that results in psychomotor retardation, ataxia and seizures. A mouse model of SSADH-d (the Aldh5a1-/- mouse) was created to study the pathophysiology and treatment of SSADH-d. Aldh5a1-/- mice have psychomotor retardation and a progressive seizure phenotype results in death around P25. The present experiments tested the effects of a ketogenic diet in the treatment of Aldh5a1-/- mice. The KD was found to prolong the lives of Aldh5a1-/- mice by >300% while significantly delaying the onset the ataxia and preventing weight loss that is seen in untreated Aldh5a1-/- mice. Electrophysiological recordings revealed a corresponding decrease in seizures in KD fed mutants, as compared to control diet (CD) fed mutants. We assessed spontaneous miniature postsynaptic currents (mPSC) in CD and KD fed mutants. We found that CD fed mutants had significantly decreased inhibitory mPSC (mIPSC) activity compared to CD fed wildtype controls. mIPSC activity was restored in KD fed Aldh5a1-/- mice. A similar effect was found in [35S]TBPS binding experiments. TBPS binding was significantly reduced in CD fed Aldh5a1-/- mice, but restored in KD fed mutants. Plasma analysis revealed that an elevation of serum beta-hydroxybutyrate may play a role in the KD’s effects. The KD led to a significant elevation in the number of hippocampal mitochondria in mutant mice. Further, the KD was able to normalize the deficiencies in the hippocampal ATP levels seen in the Aldh5a1-/- mice. The present data suggest that the KD is able to significantly improve the Aldh5a1-/- phenotype. The effect of the KD on mIPSC activity is novel and furthers our understanding of how the KD may exert its effects. The mitochondrial studies confirm the findings of others, that the KD elevates the number of mitochondria. The KD also restores ATP deficiencies in Aldh5a1-/- mice, which is a novel finding. Together, these show that the KD may be an effective treatment for SSADH-d in humans. These data also further our understanding of the KD’s mechanisms of action.

Succinic semialdehyde dehydrogenase (ALDH5A1) deficiency (SSADH-d) is an autosomal recessive, inborn error of gamma-aminobutyric acid (GABA) metabolism that results in psychomotor retardation, ataxia and seizures. A mouse model of SSADH-d (the Aldh5a1-/- mouse) was created to study the pathophysiology and treatment of SSADH-d. Aldh5a1-/- mice have psychomotor retardation and a progressive seizure phenotype results in death around P25. The present experiments tested the effects of a ketogenic diet in the treatment of Aldh5a1-/- mice. The KD was found to prolong the lives of Aldh5a1-/- mice by >300% while significantly delaying the onset the ataxia and preventing weight loss that is seen in untreated Aldh5a1-/- mice. Electrophysiological recordings revealed a corresponding decrease in seizures in KD fed mutants, as compared to control diet (CD) fed mutants. We assessed spontaneous miniature postsynaptic currents (mPSC) in CD and KD fed mutants. We found that CD fed mutants had significantly decreased inhibitory mPSC (mIPSC) activity compared to CD fed wildtype controls. mIPSC activity was restored in KD fed Aldh5a1-/- mice. A similar effect was found in [35S]TBPS binding experiments. TBPS binding was significantly reduced in CD fed Aldh5a1-/- mice, but restored in KD fed mutants. Plasma analysis revealed that an elevation of serum beta-hydroxybutyrate may play a role in the KD’s effects. The KD led to a significant elevation in the number of hippocampal mitochondria in mutant mice. Further, the KD was able to normalize the deficiencies in the hippocampal ATP levels seen in the Aldh5a1-/- mice. The present data suggest that the KD is able to significantly improve the Aldh5a1-/- phenotype. The effect of the KD on mIPSC activity is novel and furthers our understanding of how the KD may exert its effects. The mitochondrial studies confirm the findings of others, that the KD elevates the number of mitochondria. The KD also restores ATP deficiencies in Aldh5a1-/- mice, which is a novel finding. Together, these show that the KD may be an effective treatment for SSADH-d in humans. These data also further our understanding of the KD’s mechanisms of action.

Influence of food allergy and importance of diet therapy for children with atopic dermatitis Atopinis dermatitas yra dažna vaikų lėtinė odos liga, kuri sparčiai plinta visame pasaulyje [304, 369, 370]. Lietuvos mokslininkų duomenimis, atopinis dermatitas nustatytas apie 4-17% vaikų, gyvenančių Lietuvoje [38, 92]. Vienas svarbiausių atopinio dermatito patogenezės veiksnių yra alergija maistui. Įvairūs mokslininkai nurodo, kad 35-80% atopiniu dermatitu sergančių vaikų yra alergiški maistui [13, 40, 82]. Dažniausiai, atsižvelgiant į vaiko amžių, šeimą ir šalies mitybos tradicijas, kiekvienas alergiškas vaikas yra jautrus skirtingiems maisto produktams. Daugelio mokslininkų duomenimis, maisto alergenai – pienas, soja, kiaušiniai, kviečiai, riešutai ir žuvis – apibūdinami kaip vieni pagrindinių, sąlygojančių atopinio dermatito atsiradimą [48, 292]. Dauguma alergijų maistui kyla per pirmuosius 3 – 4 gyvenimo metus, kuomet virškinimo sistemos barjeras yra dar nesubrendęs, o imuninė sistema dar tobulinama gebėjimui toleruoti maistą. Visa tai lemia vaikų virškinimo sistemos reakciją į atskirus maisto produktus ir sukelia įvairius virškinimo sistemos sutrikimus [175, 288, 294]. Kiekvienam atopiniu dermatitu sergančiam vaikui labai svarbu išaiškinti jį alergizuojančius maisto produktus ir skirti dietą, kurioje ne tik nebūtų alergizuojančių maisto produktų, bet kuri užtikrintų pagrindinių maisto medžiagų, vitaminų, mineralinių medžiagų ir energijos reikiamą paros poreikį ir normalų... [to full text]

Den här uppsatsen behandlar ett antal individer begravda mellan 800 e.Kr. och 1150 e.Kr i ett tidigt kristet gravfält kring ruinen av Varnhems gårdskyrka. Av speciellt intresse är den placeringen som gravarna har i förhållande till kyrkomurarna och vad dessa placeringar innebär statusmässigt. Analys av stabila isotoper har därför utförts på de manliga individerna  så att deras diet kan faställas och agera som en markör för vad som känneteckas som hög och lågstatus bland de begravda männen i Varnhem.

Sperm whales (Physeter macrocephalus) are widely distributed in all oceans, but principally found in areas of high primary productivity. Historically, they were whaled extensively in the Sargasso Sea and recent surveys have also found large numbers there. However, the Sargasso Sea is an oceanic gyre considered to be low in productivity. This dissertation explores the paradox of a high abundance of large top predators in a body of water once described as an “oceanic desert”. First, I compared the diet of sperm whales in the Sargasso Sea to those off Dominica, in the eastern Caribbean. Results suggested differences in trophic ecology between these two areas, with sperm whales in the Sargasso Sea feeding at a higher trophic level. Second, I examined the spatial and temporal distribution of sperm whales in the Sargasso Sea in relation to environmental variables using acoustic surveys and autonomous recording devices. Sperm whale prevalence around Kelvin seamount, part of the New England Seamount Chain, was higher in the spring compared to the winter. Habitat modeling results suggest that the mesoscale activity associated with the Gulf Stream plays an important role in sperm whale occurrence in this area, likely due to the enhancement of primary productivity in this region. Finally, I estimated the current density of sperm whales in the northwestern Sargasso Sea and compared their present distribution to their distribution during the open-boat whaling era (1775-1921). Sperm whale density in the northern Sargasso Sea is one of the highest found globally, showing that this region remains a hotspot for sperm whales. The area where sperm whale detections per unit effort is presently the highest showed little overlap with areas where whales were hunted historically. Whalers all but ignored this region except when transiting to other whaling grounds, perhaps a result of fixed whaling patterns due to the conservative use of knowledge at that time. My dissertation highlights patterns and processes that help to explain the presence and abundance of sperm whales in the Sargasso Sea and demonstrates the importance of western boundary currents, such as the Gulf Stream, to the distribution of marine top predators.

Chronic kidney disease (CKD) is a worldwide health problem with rising incidence and high cardiovascular mortality. CKD compromises cardiovascular function, in part, characterized by vascular calcification (VC), elevated pulse wave velocity (PWV) and pulse pressure (PP). Through manipulation of dietary adenine, we produced a model characterized by graded severity of CKD, VC and hyperphosphatemia. To our knowledge, we are the first to explore the relationship between aortic calcium content and changes in circulatory function in rodents with CKD. Fourteen-week old Sprague-Dawley rats received a diet containing an adenine concentration (0.25-0.75%) plus high-normal dietary phosphate (1%), for up to 10 weeks. Circulatory changes were determined by arterial radiotelemetry (n=6) and by assessment of aortic pulse wave velocity (PWV, n=32). VC was assessed using the calcium-O-cresophthalein-complexone assay. At sacrifice, kidney function (creatinine (µmol/L)) was worst in the group with VC (251.3±60.2 µmol/L), compared to non-calcifying CKD (200.3±68.8 µmol/L) or control (50.0±16.2 µmol/L). PWV (cm/s) adjusted for blood pressure (BP) was markedly elevated in animals with VC (3.23±0.33 log(cm/s)) versus non-calcifying CKD (2.85± 0.12 log(cm/s)) or control (2.96±0.08 log(cm/s)). Arterial pressure radiotelemetry revealed that there was an increase in pulse pressure (38±4.7 mmHg to 58 ±15.2 mmHg) during the development of VC. Systolic pressure remained relatively stable throughout (129±8.7 mmHg), diastolic pressure fell during weeks 9 and 10 of the study (91±6.0 mmHg down to 74±9.1 mmHg), a fall that almost fully accounted for the changes in pulse pressure. The calcifying CKD animals also exhibited left ventricular hypertrophy (LVH) compared to CKD or control animals (2.32±0.3 vs 2.03±0.2, 1.80±0.1 g/kg respectively). Manipulating dietary adenine produces a graded severity of CKD with calcification which impact circulatory changes (PP and PWV). These altered circulatory functions are likely to be key factors in the enhanced LVH. This model appears to be a useful for the study of CKD-associated VC. / Thesis (Master, Pharmacology & Toxicology) -- Queen's University, 2009-12-16 15:10:49.384

The number of obese youth in Canada has tripled over the past 30 years. Two contributing factors to obesity are physical inactivity and poor nutrition. To improve these negative health behaviours, the factors that contribute to their development must be understood and intervened upon. Researchers are focusing on the built environment as one potential factor. The built environment refers to human made physical structures and infrastructure of communities that can influence health behaviours. These include the roads, buildings, parks and recreation facilities, and food retailers of which people can use through work, play, or eating. The purpose of this thesis was to determine how the built environment influences physical inactivity and fast food consumption in 11-15-year-old Canadians. Physical inactivity and fast food consumption were assessed in a national study called the Canadian Health Behaviour in School Aged Children Survey. Over 6000 youth in grades 6 to 10 were examined. Information on several built environment features were obtained in the neighbourhoods of these 6000 youth using Geographic Information Systems. Measures included walkability indices, parks and other outdoor play spaces, recreation facilities, aesthetics, and fast food restaurants. Relationships between behaviours (physical inactivity, excessive fast food consumption) and neighbourhood built environments were examined using complex statistical tests. Results indicated that youth living in highly walkable neighbourhoods, neighbourhoods with few or no cul-de-sacs, and neighbourhoods with a modest amount of park space were most likely to be physically inactive. Youth living in neighbourhoods with a moderate or high density of fast food restaurants were more likely to be excessive fast food consumers than youth living in neighbourhoods with no fast food restaurants. Approximately 15-30% of physical inactivity and excessive fast food consumption within the population was attributed to features of the neighbourhood built environment. This thesis demonstrates that several features of the neighbourhood built environment influence obesity-related health behaviours in youth. Results may guide future policy development and intervention research targeting the built environment. / Thesis (Master, Kinesiology & Health Studies) -- Queen's University, 2012-08-01 22:35:22.486