High-fat diet induced changes in lumbar vertebra of the male rat offsprings

2016 ◽  
Vol 118 (7) ◽  
pp. 711-721 ◽  
Author(s):  
Zeljka Peric Kacarevic ◽  
Darija Snajder ◽  
Andela Maric ◽  
Nikola Bijelic ◽  
Olga Cvijanovic ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Lumbar Vertebra ◽  
Male Rat ◽  
High Fat ◽  
Induced Changes

scholarly journals The Effect of Neonatal Leptin Antagonism in Male Rat Offspring Is Dependent upon the Interaction between Prior Maternal Nutritional Status and Post-Weaning Diet

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
J. Beltrand ◽  
D. M. Sloboda ◽  
K. L. Connor ◽  
M. Truong ◽  
M. H. Vickers
Keyword(s):  
High Fat Diet ◽  
Experimental Studies ◽  
Male Rat ◽  
Obesity Risk ◽  
High Fat ◽  
Maternal Nutritional Status ◽  
Rat Offspring ◽  
Pregnancy And Lactation ◽  
Induced Changes ◽  
Plasma Leptin

Epidemiological and experimental studies report associations between overweight mothers and increased obesity risk in offspring. It is unclear whether neonatal leptin regulation mediates this association between overweight mothers and offspring obesity. We investigated the effect of neonatal treatment with a leptin antagonist (LA) on growth and metabolism in offspring of mothers fed either a control or a high fat diet. Wistar rats were fed either a control (CON) or a high fat diet (MHF) during pregnancy and lactation. Male CON and MHF neonates received either saline (S) or a rat-specific pegylated LA on days 3, 5, and 7. Offspring were weaned onto either a control or a high fat (hf) diet. At day 100, body composition, blood glucose,β-hydroxybutyrate and plasma leptin and insulin were determined. In CON and MHF offspring, LA increased neonatal bodyweights compared to saline-treated offspring and was more pronounced in MHF offspring. In the post-weaning period, neonatal LA treatment decreased hf diet-induced weight gain but only in CON offspring. LA treatment induced changes in body length, fat mass, body temperature, and bone composition. Neonatal LA treatment can therefore exert effects on growth and metabolism in adulthood but is dependent upon interactions between maternal and post-weaning nutrition.

scholarly journals Characterizing the Retinal Phenotype in the High-Fat Diet and Western Diet Mouse Models of Prediabetes

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 464 ◽  
Author(s):  
Bright Asare-Bediako ◽  
Sunil Noothi ◽  
Sergio Li Calzi ◽  
Baskaran Athmanathan ◽  
Cristiano Vieira ◽  
...  
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Fundus Photography ◽  
Vascular Density ◽  
Sensitivity Index ◽  
High Fat ◽  
Permeability Studies ◽  
Induced Changes ◽  
Acellular Capillaries

We sought to delineate the retinal features associated with the high-fat diet (HFD) mouse, a widely used model of obesity. C57BL/6 mice were fed either a high-fat (60% fat; HFD) or low-fat (10% fat; LFD) diet for up to 12 months. The effect of HFD on body weight and insulin resistance were measured. The retina was assessed by electroretinogram (ERG), fundus photography, permeability studies, and trypsin digests for enumeration of acellular capillaries. The HFD cohort experienced hypercholesterolemia when compared to the LFD cohort, but not hyperglycemia. HFD mice developed a higher body weight (60.33 g vs. 30.17g, p < 0.0001) as well as a reduced insulin sensitivity index (9.418 vs. 62.01, p = 0.0002) compared to LFD controls. At 6 months, retinal functional testing demonstrated a reduction in a-wave and b-wave amplitudes. At 12 months, mice on HFD showed evidence of increased retinal nerve infarcts and vascular leakage, reduced vascular density, but no increase in number of acellular capillaries compared to LFD mice. In conclusion, the HFD mouse is a useful model for examining the effect of prediabetes and hypercholesterolemia on the retina. The HFD-induced changes appear to occur slower than those observed in type 2 diabetes (T2D) models but are consistent with other retinopathy models, showing neural damage prior to vascular changes.

scholarly journals Identification of Sox2 and NeuN Double-Positive Cells in the Mouse Hypothalamic Arcuate Nucleus and Their Reduction in Number With Aging

2021 ◽  
Vol 12 ◽  
Author(s):  
Ayumu Sugiura ◽  
Tatsuhiro Shimizu ◽  
Takeshi Kameyama ◽  
Tomohiko Maruo ◽  
Shin Kedashiro ◽  
...  
Keyword(s):  
Stem Cells ◽  
High Fat Diet ◽  
Arcuate Nucleus ◽  
High Fat ◽  
Double Positive ◽  
Diet Induced Obesity ◽  
Hypothalamic Arcuate Nucleus ◽  
Hypothalamic Cells ◽  
Induced Changes ◽  
Insight Into

The hypothalamus plays a central role in homeostasis and aging. The hypothalamic arcuate nucleus (ARC) controls homeostasis of food intake and energy expenditure and retains adult neural stem cells (NSCs)/progenitor cells. Aging induces the loss of NSCs and the enhancement of inflammation, including the activation of glial cells in the ARC, but aging-associated alterations of the hypothalamic cells remain obscure. Here, we identified Sox2 and NeuN double-positive cells in a subpopulation of cells in the mouse ARC. These cells were reduced in number with aging, although NeuN-positive neuronal cells were unaltered in the total number. Diet-induced obesity mice fed with high-fat diet presented a similar hypothalamic alteration to aged mice. This study provides a new insight into aging-induced changes in the hypothalamus.

High fat diet induced changes in gastric vagal afferent response to adiponectin

2015 ◽  
Vol 152 ◽  
pp. 354-362 ◽  
Author(s):  
Stephen J. Kentish ◽  
Kyle Ratcliff ◽  
Hui Li ◽  
Gary A. Wittert ◽  
Amanda J. Page
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Vagal Afferent ◽  
Induced Changes ◽  
Afferent Response

scholarly journals Effect of stevia on the gut microbiota and glucose tolerance in a murine model of diet-induced obesity

2020 ◽  
Vol 96 (6) ◽  
Author(s):  
Sarah L Becker ◽  
Edna Chiang ◽  
Anna Plantinga ◽  
Hannah V Carey ◽  
Garret Suen ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Gut Microbiota ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Treatment Groups ◽  
Low Fat Diet ◽  
Taxonomic Groups ◽  
Induced Changes

ABSTRACT Artificial sweeteners have been shown to induce glucose intolerance by altering the gut microbiota; however, little is known about the effect of stevia. Here, we investigate whether stevia supplementation induces glucose intolerance by altering the gut microbiota in mice, hypothesizing that stevia would correct high fat diet-induced glucose intolerance and alter the gut microbiota. Mice were split into four treatment groups: low fat, high fat, high fat + saccharin and high fat + stevia. After 10 weeks of treatment, mice consuming a high fat diet (60% kcal from fat) developed glucose intolerance and gained more weight than mice consuming a low fat diet. Stevia supplementation did not impact body weight or glucose intolerance. Differences in species richness and relative abundances of several phyla were observed in low fat groups compared to high fat, stevia and saccharin. We identified two operational taxonomic groups that contributed to differences in beta-diversity between the stevia and saccharin groups: Lactococcus and Akkermansia in females and Lactococcus in males. Our results demonstrate that stevia does not rescue high fat diet-induced changes in glucose tolerance or the microbiota, and that stevia results in similar alterations to the gut microbiota as saccharin when administered in concordance with a high fat diet.

scholarly journals Postnatal Dietary Omega-3 Fatty Acid Supplementation Rescues Glucocorticoid-Programmed Adiposity, Hypertension, and Hyperlipidemia in Male Rat Offspring Raised on a High-Fat Diet

Endocrinology ◽  
2013 ◽  
Vol 154 (9) ◽  
pp. 3110-3117 ◽  
Author(s):  
Intan S. Zulkafli ◽  
Brendan J. Waddell ◽  
Peter J. Mark
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
High Fat Diet ◽  
Plasma Cholesterol ◽  
Adverse Outcomes ◽  
Male Rat ◽  
Delayed Puberty ◽  
Adult Offspring ◽  
Omega 3 ◽  
High Fat

Fetal glucocorticoid excess programs several adverse outcomes in adult offspring, many of which can be prevented by postnatal, dietary omega-3 (n-3) fatty acids. Here we tested 2 separate hypotheses: 1) a postnatal high-fat diet exacerbates the glucocorticoid-programmed phenotype; and 2) postnatal, dietary n-3 fatty acids rescue programmed outcomes, even in the presence of a high-fat diet challenge. Pregnant Wistar rat dams were either untreated or administered dexamethasone acetate (Dex; 0.5 μg/mL drinking water) from day 13 of pregnancy. Offspring were cross-fostered to untreated mothers and males were weaned onto a standard (Std), high-fat, low n-3 (HF), or high-fat, high n-3 (HFHn-3) diet. Prenatal Dex reduced birth weight (26%) and delayed puberty onset by 1.2 days, irrespective of postnatal diet. Prenatal Dex programmed increased blood pressure in adult offspring, an effect worsened by the postnatal HF diet. Supplementation with high n-3 fatty acids, however, prevented both the Dex and HF-induced increases in blood pressure. Prenatal Dex also programmed increased adiposity, plasma cholesterol, and plasma triglyceride levels at 6 months of age, particularly in those offspring raised on the HF diet. But again, each of these adverse outcomes was rescued by supplementation of the HF diet with n-3 fatty acids. In conclusion, the capacity of n-3 fatty acids to overcome adverse programming outcomes remains evident, even in the presence of a HF diet challenge.

Aryl hydrocarbon receptor-deficient mice are protected from high fat diet-induced changes in metabolic rhythms

2017 ◽  
Vol 34 (3) ◽  
pp. 318-336 ◽  
Author(s):  
Cassie Jaeger ◽  
Canxin Xu ◽  
Mingwei Sun ◽  
Stacey Krager ◽  
Shelley A. Tischkau
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
High Fat Diet ◽  
High Fat ◽  
Aryl Hydrocarbon ◽  
Induced Changes ◽  
Deficient Mice
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