Table 3 - uploaded by Elizabeth Rendina-Ruedy
Content may be subject to copyright.
Source publication
The prevalence of obesity and type 2 diabetes mellitus (T2DM) continues to rise, and as a result, research aimed at understanding the molecular basis for the co-morbidities has become an area of much scientific interest. Among the more recently recognized chronic complications of T2DM is the increased risk of fracture, especially hip fracture, that...
Context in source publication
Context 1
... fatty acid profile of lard is B37% saturated (sFA), 46% monounsaturated (MUFAs), and 17% polyunsaturated (PUFAs) (Note 6). Lard has particularly high amounts of palmitic, steric and oleic acid ( Table 3). It is important for researchers to take note that not all high-fat diets at a given percentage of kcal are created equal and the additional fat source is of particular relevance. ...
Similar publications
Diet-induced obesity (DIO) resulting from consumption of a high fat diet (HFD) attenuates normal neuronal responses to leptin and may contribute to the metabolic defense of an acquired higher body weight in humans; the molecular bases for the persistence of this defense are unknown. We measured the responses of 23 brain regions to exogenous leptin...
Citations
... Additionally, the composition of the diet could influence the expression of this enzyme. In this respect, it has been demonstrated that food rich in unsaturated fatty acids such as soybean oil and lard 76 , reduces SREBP-1c and FASN levels in hepatocytes 77,78 . Analysis of the expression of SCD-1, the key enzyme in the synthesis of the monounsaturated fatty acids (MUFAs) oleicand palmitoleic acids, revealed considerably reduced levels of this enzyme in liver tissue from mice exposed to CX-4945 but not in eWAT. ...
... Lard contains extremely high levels of oleic acid (44%), palmitic acid (27%) and stericand oleic acid (11%). 16 Because of the composition, lard has been recommended and a commonly used as fat source in metabolic studies on mice. These diets have been particularly effective in mimicking the metabolic effects of the human diet due to the significant proportion of lard consumption in human diets in the world. ...
Pork is one type of the most frequently consumed meat with about 30% globally. Thus, the questions regarding to the health effects of diet with high fat content from lard are raised. Here, we developed a model of mice fed with high fat (HF) from lard to investigate and have more insights on the effects of long-time feeding with HF on health. The results showed that 66 days on HF induced a significant gain in the body weight of mice, and this weight gain was associated to the deposits in the white fat, but not brown fat. The glucose tolerance, not insulin resistance, in mice was decreased by the HF diet, and this was accompanied with significantly higher blood levels of total cholesterol and triglycerides. Furthermore, the weight gains in mice fed with HF seemed to link to increased mRNA levels of adipose biomarkers in lipogenesis, including Acly and Acaca genes, in white fat tissues. Thus, our study shows that a diet with high fat from lard induced the increase in body weight, white fat depots’ expansion, disruption of glucose tolerance, blood dyslipidemia, and seemed to start affecting the mRNA expression of some adipose biomarkers in a murine model.
... In addition to the paucity of information about the effect of DIO on the fracture resistance of bone, we do not know if the HFD alone or the resulting glucose intolerance is responsible for bone fragility. Most published mouse studies using DIO to investigate diabetic effects on bone involved C57BL/6 mice (sub-strain, J or N, not always being clear) since this widely available inbred strain becomes glucose intolerant, especially when fed a HFD starting at a young age (3-6 weeks-old) [30]. Since most DIO studies started HFD in growing mice, the effect of T2D on bone in adult mice is less clear. ...
Obesity and type 2 diabetes (T2D) are risk factors for fragility fractures. It is unknown whether this elevated risk is due to a diet favoring obesity or the diabetes that often occurs with obesity. Therefore, we hypothesized that the fracture resistance of bone is lower in mice fed with a high fat diet (45% kcal; HFD) than in mice that fed on a similar, control diet (10% kcal; LFD), regardless of whether the mice developed overt T2D. Sixteen-week-old, male NON/ShiLtJ mice (resistant to T2D) and age-matched, male NONcNZO10/LtJ (prone to T2D) received a control LFD or HFD for 21 weeks. HFD increased the bodyweight to a greater extent in the ShiLtJ mice compared to the NZO10 mice, while blood glucose levels were significantly higher in NZO10 than in ShiLtJ mice. As such, the glycated hemoglobin A1c (HbA1c) levels exceeded 10% in NZO10 mice, but it remained below 6% in ShiLtJ mice. Diet did not affect HbA1c. HFD lowered trabecular number and bone volume fraction of the distal femur metaphysis (micro-computed tomography or μCT) in both strains. For the femur mid-diaphysis, HFD significantly reduced the yield moment (mechanical testing by three-point bending) in both strains but did not affect cross-sectional bone area, cortical thickness, nor cortical tissue mineral density (μCT). Furthermore, the effect of diet on yield moment was independent of the structural resistance of the femur mid-diaphysis suggesting a negative effect of HFD on characteristics of the bone matrix. However, neither Raman spectroscopy nor assays of advanced glycation end-products identified how HFD affected the matrix. HFD also lowered the resistance of cortical bone to crack growth in only the diabetic NZO10 mice (fracture toughness testing of other femur), while HFD reduced the ultimate force of the L6 vertebra in both strains (compression testing). In conclusion, the HFD-related decrease in bone strength can occur in mice resistant and prone to diabetes indicating that a diet high in fat deleteriously affects bone without necessarily causing hyperglycemia.
... PUFAs are susceptible to degradation. Lard, a major component of HF diets, contains a significant proportion of unsaturated fatty acids, which are prone to oxidization [28]. Lipid peroxidation in the TCP diets was two to three times higher than in the DCM and CCBR diets (Supplemental Table S2). ...
The environment of the test laboratory affects the reproducibility of treatment effects on physiological phenotypes of rodents and may be attributed to the plasticity of the epigenome due to nutrient-gene-environment interactions. Here, we explored the reproducibility of adding a multi-vitamin-mineral (MVM) mix to a nutrient-balanced high-fat (HF) diet on obesity, insulin resistance (IR), and gene expression in the tissues of adult male mice. Experiments of the same design were conducted in three independent animal facilities. Adult C57BL/6J male mice were fed an HF diet for 6 weeks (diet induced-obesity model) and then continued for 9–12 weeks on the HF diet with or without 5-fold additions of vitamins A, B1, B6, B12, Zn, and 2-fold Se. The addition of the MVM affected body weight, fat mass, gene expression, and markers of IR in all three locations (p < 0.05). However, the direction of the main effects was influenced by the interaction with the experimental location and its associated environmental conditions known to affect the epigenome. In conclusion, MVM supplementation influenced phenotypes and expression of genes related to adipose function in obese adult male mice, but the experimental location and its associated conditions were significant interacting factors. Preclinical studies investigating the relationship between diet and metabolic outcomes should acknowledge the plasticity of the epigenome and implement measures to reproduce studies in different locations.
... This ratio was maintained across the HF diets to match the fatty acid profile between LF and HF diets. Based on previously published fatty acid profiles of soybean oil and lard, 46 the modified AIN-93G (LF) diet included ∼15 g kg −1 of n-6 fatty acids, which meets the recommended requirement for essential fatty acids for growth of rats. 47 The diet containing whole red wheat consisted of 45.5% wheat flour by weight. ...
We previously found greater reduction of colon cancer (CC) biomarkers for red wheat compared to white wheat regardless of refinement state. In the present study we examined whether the phenolic-rich aleurone and testa layers are drivers of chemoprevention by red wheat and their influence on gut microbiota composition using a 1,2-dimethylhydrazine-induced CC rat model. Rats were fed a low-fat diet (16% of energy as fat), high-fat diet (50% of energy as fat), or high-fat diet containing whole red wheat, refined red wheat, refined white wheat, or aleurone- or testa-enriched fractions for 12 weeks. Morphological markers (aberrant crypt foci, ACF) were assessed after methylene blue staining and biochemical markers (3-nitrotyrosine [3-NT], Dclk1) by immunohistochemical determination of staining positivity within aberrant crypts. Gut microbiota composition was evaluated from 16S rRNA gene sequencing of DNA extracted from cecal contents. Relative to the high-fat diet, the whole and refined red wheat, refined white wheat, and testa-enriched fraction decreased ACF, while only the refined red wheat and aleurone-enriched fraction decreased 3-NT. No significant differences were observed for Dclk1. An increase in microbial diversity was observed for the aleurone-enriched fraction (ACE index) and whole red wheat (Inverse Simpson Index). The diet groups significantly modified overall microbiome composition, including altered abundances of Lactobacillus, Mucispirillum, Phascolarctobacterium, and Blautia coccoides. These results suggest that red wheat may reduce CC risk through modifications to the gut microbiota and nitrosative stress, which may be due, in part, to the influence of dietary fiber and the phenolic-rich aleurone layer.
... In the experiments described above, dietary fat was sourced from plant-based soy oil. Plant oils have a relatively lower saturated fat content (especially palmitic acid) than animal fats 26 . Therefore, we investigated if replacing soy oil with lard altered the nature of fatfructose-glucose interaction and the associated metabolic outcomes. ...
The metabolic effects of sugars and fat lie at the heart of the “carbohydrate vs fat” debate on the global obesity epidemic. Here, we use nutritional geometry to systematically investigate the interaction between dietary fat and the major monosaccharides, fructose and glucose, and their impact on body composition and metabolic health. Male mice (n = 245) are maintained on one of 18 isocaloric diets for 18–19 weeks and their metabolic status is assessed through in vivo procedures and by in vitro assays involving harvested tissue samples. We find that in the setting of low and medium dietary fat content, a 50:50 mixture of fructose and glucose (similar to high-fructose corn syrup) is more obesogenic and metabolically adverse than when either monosaccharide is consumed alone. With increasing dietary fat content, the effects of dietary sugar composition on metabolic status become less pronounced. Moreover, higher fat intake is more harmful for glucose tolerance and insulin sensitivity irrespective of the sugar mix consumed. The type of fat consumed (soy oil vs lard) does not modify these outcomes. Our work shows that both dietary fat and sugars can lead to adverse metabolic outcomes, depending on the dietary context. This study shows how the principles of the two seemingly conflicting models of obesity (the “energy balance model” and the “carbohydrate insulin model”) can be valid, and it will help in progressing towards a unified model of obesity. The main limitations of this study include the use of male mice of a single strain, and not testing the metabolic effects of fructose intake via sugary drinks, which are strongly linked to human obesity.
... While some investigators rely on genetically modified transgenic and congenic mouse models, others utilize nutritional interventions in the form of high fat diets. We have previously provided an in-depth review regarding this model system (40). When performing these studies some key considerations include percent fat of diet, fat source, compensatory carbohydrate source of the control diet (i.e., added fat decreases the proportion of carbohydrate and/or protein), feeding schedule, and food/calorie intake. ...
Bone is a highly dynamic tissue that undergoes continuous remodeling by bone resorbing osteoclasts and bone forming osteoblasts, a process regulated in large part by osteocytes. Dysregulation of these coupled catabolic and anabolic processes as in the case of menopause, type 2 diabetes mellitus, anorexia nervosa, and chronic kidney disease is known to increase fracture risk. Recent advances in the field of bone cell metabolism and bioenergetics have revealed that maintenance of the skeleton places a high energy demand on these cells involved in bone remodeling. These new insights highlight the reason that bone tissue is the beneficiary of a substantial proportion of cardiac output and post-prandial chylomicron remnants and requires a rich supply of nutrients. Studies designed for the specific purpose of investigating the impact of dietary modifications on bone homeostasis or that alter diet composition and food intake to produce the model can be found throughout the literature; however, confounding dietary factors are often overlooked in some of the preclinical models. This review will examine some of the common pre-clinical models used to study skeletal biology and its pathologies and the subsequent impact of various dietary factors on these model systems. Furthermore, the review will include how inadvertent effects of some of these dietary components can influence bone cell function and study outcomes.
... En fonction du type de graisse la composition finale en acides gras saturés, polyinsaturés, monoinsaturés et en omégas-3 et 6 va grandement varier, ainsi que leurs conséquences sur la santé. Il est difficile de définir un régime sur-gras « idéal » et la grande variété de formules disponibles se traduit par une grande variabilité entre les études[254]. Par exemple l'huile de palme induit une plus forte expression d'IL-6 dans le plasma sanguin et une plus forte expression d'IL-1β, TLR4 et CD14 dans le tissus adipeux par rapport à l'huile de colza, l'huile de tournesol ou le beurre[255].En général les régimes sur-gras faits à partir de graisses animales comme le beurre, le lard ou une autre source importante d'acides gras saturés conduisent à une prise de poids et une stéatose hépatique plus prononcées par rapport aux régimes sur-gras principalement composés d'huiles végétales ou d'huile de poisson[256][257][258][259].59 ...
Le microbiote intestinal est un écosystème de microorganismes dont les nombreuses fonctions digestives et immunitaires le rendent indispensable à la bonne santé de son hôte. Une susceptibilité génétique associée à des perturbations environnementales peut rompre cet équilibre et entrainer une dysbiose. L’inflammation chronique en résultant se traduit en différents troubles locaux et systémiques. Ainsi la dysbiose a été mise en cause dans la physiopathologie des maladies inflammatoires chroniques de l’intestin et également au développement de troubles métaboliques associés à l’obésité.Les peptides antimicrobiens sont des molécules du système immunitaire innée ayant des fonctions de contrôle de la population bactérienne au niveau de la barrière intestinale et empêchant le contact direct entre celles-ci et les cellules épithéliales.L’objectif de cette thèse est d’étudier le potentiel thérapeutique des peptides antimicrobiens dans le traitement de maladies liées à la dysbiose comme les MICI et le syndrome métabolique. Pour cela Lactococcus lactis, une bactérie lactique interagissant de manière transitoire avec la barrière épithéliale intestinale, a été utilisée comme vecteur de la molécule d’intérêt. Durant cette thèse j’ai pu établir que la cathélicidine humaine (hCAP18) et REG3A avaient un impact sur le microbiote et amélioraient les symptômes de la colite induite et de l’obésité chez le rongeur.
... Coconut oil contains 90% sFA, 2% MUFAs and 4% PUFAs. The fatty acid profile of coconut oil indicates high levels of lauric, myristic, capric, and caprylic acid, which differ significantly from lard (Rendina-Ruedy & Smith, 2016). ...
The alginate beads encapsulated thyme (AT), rosemary (AR) and geranium (AG) essential oils (EOs) were prepared to inhibit lipid oxidation in lard and coconut oil. The result showed that beads dried in hot air oven (45 °C) encapsulated higher amount of EOs than drying by desiccation method. Sachets containing AT, AR and AG were applied in PET bottles containing lard and coconut oils and stored at 45 °C. The DPPH scavenging activities of AT, AR and AG were 85.39%, 78.26%, and 78.12%, respectively. During storage, released EOs reduced PV and TBARS of lard and coconut oil and did not affect their colour acceptability scores. From PV, FFA and TBARS, AT at 0.50 g exhibited the best results in terms of lipid oxidation inhibition, although encapsulation percentage and release were significantly lower than AG and AR. Porous in alginate beads could entrap lipid oxidation products, including volatile compounds and water vapour. Besides, the hydrophilic property of polymer matrix led to water absorption, which lower aw value. In week3, the odour acceptability scores of control lard failed, while those packed with AT, AR and AG were acceptable. Alginate beads containing EOs can be used to extend the storage life of lard and coconut oil.
... The main saturated fatty acid in lard is palmitic acid and it does not contain any lauric acid. The main unsaturated fatty acid in lard is also oleic acid, but the amount is several times higher (44%) than in coconut oil (7%) 70 . There was very little variation in the survival of DGRP strains on the high-lard diet, and moreover, this diet led to faster development in most of the strains tested. ...
Carbohydrates, proteins and lipids are essential nutrients to all animals; however, closely related species, populations, and individuals can display dramatic variation in diet. Here we explore the variation in macronutrient tolerance in Drosophila melanogaster using the Drosophila genetic reference panel, a collection of ~200 strains derived from a single natural population. Our study demonstrates that D. melanogaster, often considered a “dietary generalist”, displays marked genetic variation in survival on different diets, notably on high-sugar diet. Our genetic analysis and functional validation identify several regulators of macronutrient tolerance, including CG10960/GLUT8, Pkn and Eip75B. We also demonstrate a role for the JNK pathway in sugar tolerance and de novo lipogenesis. Finally, we report a role for tailless, a conserved orphan nuclear hormone receptor, in regulating sugar metabolism via insulin-like peptide secretion and sugar-responsive CCHamide-2 expression. Our study provides support for the use of nutrigenomics in the development of personalized nutrition. Responses to diet composition may be linked to susceptibility to metabolic diseases such as type 2 diabetes. Here the authors report that Drosophila melanogaster displays genetic variation in survival on different diets and describe the importance for JNK-pathway and a conserved orphan nuclear hormone receptor tailless in regulating sugar tolerance.