Impaired microvascular insulin signaling may develop before overt indices of microvascular endothelial dysfunction and represent an early pathological feature of adolescent obesity. Using a translational porcine model of juvenile obesity, we tested the hypotheses that in the early stages of obesity development, impaired insulin signaling manifests in skeletal muscle (triceps), brain (prefrontal cortex), and corresponding vasculatures, and that depressed insulin-induced vasodilation is reversible with acute inhibition of protein kinase Cβ (PKCβ). Juvenile Ossabaw miniature swine (3.5 mo of age) were divided into two groups: lean control ( n = 6) and obese ( n = 6). Obesity was induced by feeding the animals a high-fat/high-fructose corn syrup/high-cholesterol diet for 10 wk. Juvenile obesity was characterized by excess body mass, hyperglycemia, physical inactivity (accelerometer), and marked lipid accumulation in the skeletal muscle, with no evidence of overt atherosclerotic lesions in athero-prone regions, such as the abdominal aorta. Endothelium-dependent (bradykinin) and -independent (sodium nitroprusside) vasomotor responses in the brachial and carotid arteries (wire myography), as well as in the skeletal muscle resistance and 2A pial arterioles (pressure myography) were unaltered, but insulin-induced microvascular vasodilation was impaired in the obese group. Blunted insulin-stimulated vasodilation, which was reversed with acute PKCβ inhibition (LY333-531), occurred alongside decreased tissue perfusion, as well as reduced insulin-stimulated Akt signaling in the prefrontal cortex, but not the triceps. In the early stages of juvenile obesity development, the microvasculature and prefrontal cortex exhibit impaired insulin signaling. Such adaptations may underscore vascular and neurological derangements associated with juvenile obesity.

PurposeRecent clinical data suggest an increasing prevalence of obesity and type 2 diabetes in adolescents, placing them at high risk of developing diabetic retinopathy during adult working years. The present study was designed to characterize the early retinal and microvascular alterations in young Ossabaw pigs fed a Western diet, described as a model of metabolic syndrome genetically predisposed to type 2 diabetes.MethodsFour-month-old Ossabaw miniature pigs were divided into two groups, lean and diet-induced obesity. Obese pigs were fed a Western diet with high-fat/high-fructose corn syrup/high-choleric content for 10 weeks. Blood and retina were collected for biochemical profiling, trypsin digest, flatmounts, Fluoro-Jade C staining, electron microscopy, quantitative PCR, immunohistochemistry, and Western blots.ResultsYoung Ossabaw pigs had elevated fasting blood glucose after feeding on a Western diet for 10 weeks. Their retina showed disrupted cellular architecture across neural layers, with numerous large vacuoles seen in cell bodies of the inner nuclear layer. Microvessels in the obese animals exhibited thickened basement membrane, along with pericyte ghosts and acellular capillaries. The pericyte to endothelial ratio decreased significantly. Retina flatmounts from obese pigs displayed reduced capillary density, numerous terminal capillary loops, and string vessels, which stained collagen IV but not isolectin IB4. Quantitative PCR and Western blots showed significantly high levels of basement membrane proteins collagen IV and fibronectin in obese pigs.ConclusionsThis is the first study to describe the ultrastructural neuronal and vascular changes in the retina of young Ossabaw pigs fed a Western diet, simulating early signs of diabetic retinopathy pathogenesis.

Though heat stress is becoming increasingly common in pig production, efforts are ongoing to mitigate the negative effects of heat stress on feed consumption. During a period of heat stress, 40 pigs (87.4 ± 0.86 kg) were fed oleic acid (0%, 2%, 4%, 6% and 8%, n = 8 per diet) to improve growth rate. With the rising concern for welfare issues in swine production, we sought to measure how the diet would affect lameness in growing pigs. Therefore, the objectives of this study were to 1) use thermal imaging as a noninvasive measure to detect lameness and 2) to measure effects of oleic acid on the development of osteochondritic lesions. For 6 weeks during the growing phase, visual observations for lameness were conducted by a single trained observer. Additionally, thermal imaging was performed on the lateral aspect of each leg to include the stifle or elbow joint to the foot. At 120.6 ± 1.11 kg, pigs were necropsied and evaluated for joint health by measurement of the number of lesions, total size of lesions, and cartilage score on the proximal humerus, radius/ulna, and tibia/fibula, and the distal aspect of the humerus, radius/ulna, femur, and tibia/fibula. Scoring of the cartilage was based on a 0 to 4 scale, where 0 represents no lesions, and 4 represents severely damaged cartilage. No treatment effects were observed (P > 0.10), however overall lameness scores increased as pigs aged (P < 0.01). Only pigs in the control treatment (0% oleic acid) had an overall increase in temperatures of the right and left knee (P < 0.01). No observable differences occurred in cartilage scores, total lesion size, or number of lesions (P > 0.10) regardless of joint or treatment. Further research is needed to measure if oleic acid in the diet could improve joint health.

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ObjectivesThe objective of this study was to determine the effects of feeding chestnuts and acorns on growth performance, carcass quality and further processed products of Duroc/Duroc crossbred finishing barrows.Materials and MethodsBarrows (n = 30) were individually housed in pens, blocked by body weight and randomly assigned to one of three treatments: control (n = 10), inclusion of acorns at 15% of the diet (n = 7), inclusion of chestnuts at 15% of the diet (n = 13). Pigs were fed ad libitum for 28 d prior to harvest. Feed refusal and individual pig weights were collected every 7 d and used to calculate average daily gain (ADG), gain-to-feed (G:F), and average daily feed intake (ADFi). Following harvest, carcass quality was determined by objective color (L*, a* and b*), fat composition and marbling scores. Fat samples were removed from four fat depots (backfat, seam, jowl, kidney and pelvic) and analyzed for fatty acid composition. Sample chops were removed between the 10th and 11th rib of the left side of each carcass and analyzed for fatty acid composition, moisture and fat content. Bellies were removed from the left side of each carcass, further processed into bacon slabs and analyzed for slice quality, fatty acid composition, moisture and fat content. Carcass characteristics and bacon quality were analyzed using GLM procedure of SAS. Growth performance and fatty acid composition were analyzed using MIXED procedure of SAS. Significance was determined at P-value < 0.05.ResultsNo differences were detected for ADG and ADFi across treatments (P > 0.05). Barrows fed chestnut diets had a greater G:F when compared to control (P < 0.05) or acorn fed barrows (P < 0.05). Dietary treatments did not impact (P > 0.05) carcass characteristics or carcass quality. Inclusion of chestnuts or acorns within the diet did not impact (P > 0.05) moisture and fat content of chops and bacon slices (P > 0.05). Moreover, feeding acorns led to similar concentrations (P > 0.05) of palmitoleic acid (16:1) and linoleic acid (18:2n6c) when compared to the control diet. However, feeding diets containing acorns led to greater proportions (P < 0.01) of palmitoleic acid and linoleic acid similar to barrows fed diets containing chestnuts. No difference (P > 0.05) for stearic acid (18:0) were observed between control and chestnut treatments, however, both were found to have greater amounts (P < 0.01) of stearic acid when compared to the acorn treatment. Acorns increased (P < 0.01) the total concentration of omega-6 fatty acids (n-6) when compared to chestnut diets, but no differences (P > 0.05) were observed between acorn and control diets. Inclusion of acorns reduced (P < 0.05) total saturated fatty acids (SFA) when compared to control and chestnut treatments; however total polyunsaturated fatty acids (PUFA) were increased (P < 0.05) when acorns were included in the diet. When evaluating PUFA:SFA ratio, no differences (P > 0.05) were found between control and chestnut diets. Including acorns in the diet, resulted in an increased (P < 0.05) PUFA:SFA ratio.ConclusionInclusion of acorns and chestnuts did not negatively impact carcass characteristics, carcass quality or bacon quality, nevertheless, including acorns altered overall fatty acid composition while minimal differences were observed between diets containing chestnuts and the control.