Effects of Obesity on Bone Healing in Rats

Although the association between periodontitis and obesity is well explored, it is unclear whether obesity is associated with a worse therapeutic outcome after periodontal treatment. The aim of this study was to investigate the effects of obesity on bone healing with and without the application of regeneration-promoting molecules. A standardized bone fenestration-type defect was created over the root of the mandibular first molar in 15 Wistar rats. Ten animals received a high-fat, high-sucrose diet (HFSD), while the remaining five animals were fed a standard diet. During surgery, the fenestration defects from half of the HFSD-fed, i.e., obese animals, were treated with regeneration-promoting molecules (enamel matrix derivative; EMD). After four weeks, bone healing was evaluated by histomorphometry, TRAP staining and immunohistochemistry for RUNX2 and osteopontin. The analyses revealed that the spontaneous healing of the periodontal defects was compromised by obesity. Application of EMD partially compensated for the negative effect of obesity. Nevertheless, EMD-stimulated bone healing in obese animals was not better than the spontaneous healing in the obesity-free control group, indicating that obesity may also inhibit the stimulatory effects of regeneration-promoting molecules. Our results show that obesity can negatively influence bone healing and suggest that bone healing may be compromised in humans.

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Eight-Week Consumption of High-Sucrose Diet Has a Pro-Oxidant Effect and Alters the Function of the Salivary Glands of Rats

Nutrients ◽

10.3390/nu10101530 ◽

2018 ◽

Vol 10 (10) ◽

pp. 1530 ◽

Cited By ~ 17

Author(s):

Mateusz Maciejczyk ◽

Jan Matczuk ◽

Małgorzata Żendzian-Piotrowska ◽

Wiesława Niklińska ◽

Katarzyna Fejfer ◽

...

Keyword(s):

Salivary Gland ◽

Oxidative Damage ◽

Salivary Glands ◽

Redox Balance ◽

Control Group ◽

Parotid Glands ◽

Sucrose Diet ◽

High Sucrose Diet ◽

Gland Function ◽

High Sucrose

A high-sucrose diet (HSD) is widely known for its cariogenic effects and promotion of obesity, insulin resistance, type 2 diabetes, and cancer. However, the impact of the HSD diet on the salivary gland function as well as the level of salivary oxidative stress is still unknown and requires evaluation. Our study is the first to determine both redox balance and oxidative injury in the parotid and submandibular glands of rats fed the HSD diet compared to the control group. We have demonstrated that uric acid concentration and the activity of superoxide dismutase and peroxidase varied significantly in both the submandibular and parotid glands of HSD rats vs. the control group. However, enhanced oxidative damage to proteins, lipids, and DNA (increase in advanced glycation end products, advanced oxidation protein products, 4-hydroxynonenal, and 8-hydroxy-2’-deoxyguanosine) was observed only in the parotid glands of HSD rats. Moreover, the HSD diet also reduced the total protein content and amylase activity in both types of salivary glands and decreased the stimulated salivary flow rate. To sum up, an HSD diet reduces salivary gland function and disturbs the redox balance of the parotid as well as submandibular salivary glands. However, the parotid glands are more vulnerable to both antioxidant disturbances and oxidative damage.

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Effect of High Sucrose Diet on Histopathological Indicators Associated With Nonalcoholic Fatty Liver Disease in Male and Female C57bl/6N Mice

Current Developments in Nutrition ◽

10.1093/cdn/nzab038_073 ◽

2021 ◽

Vol 5 (Supplement_2) ◽

pp. 461-461

Author(s):

Melissa Vega-Burgueño ◽

Marcela Vergara-Jiménez ◽

Lorenzo Osuna-Ramirez ◽

Edith Torres-Montoya ◽

José Zazueta-Moreno ◽

...

Keyword(s):

Inflammatory Infiltrate ◽

Metabolic Stress ◽

Research Network ◽

Standard Diet ◽

Score System ◽

Male And Female ◽

Histological Score ◽

Sucrose Diet ◽

High Sucrose Diet ◽

High Sucrose

Abstract Objectives To evaluate the effect of a high sucrose diet on the histopathological indicators related to NAFLD in male and female mice of the C57bl/6N strain. Methods Forty male and female mice of the C57bl/6N strain were randomly divided into four experimental groups: Control male (CMG) and female groups (CFG) with a standard diet (Rodent Chow) and tap water, as well as sucrose male (SMG) and female groups (SFG) which received standard diet and a 50% sucrose water solution. All the groups were fed ad libitum to one of the two different diets for 20 weeks. After 20 weeks, mice were sacrificed. Blood, hepatic and adipose tissues were collected for analyses. Hepatic tissues were sectioned and stained with hematoxylin and eosin. Samples were examined by light microscopy to analyze liver damage. The non-alcoholic steatohepatitis (NASH) degree was determined according to the histological score system proposed by the clinical research network of NASH. Results In hepatic histological samples of MCG, a normal parenchyma formed by hepatocytes with a conserved architecture was observed, in which the cytoplasm and the nucleus can be appreciated. According to the histological score system of the clinical research network of NASH, it was not considered into any NASH grade. FCG showed few microvesicles in parenchyma, developing grade 1 of NASH, with microvesicular steatosis, not considered pathological. Compared to sucrose groups, in MSG were observed presence of moderate microvesicular steatosis, moderate metabolic stress, and glycogen condensation. No presence of inflammatory infiltrate, inflammation, or granulomas, developing grade 4 of NASH. On the other hand, FSG showed a wide spread of macrovesicular steatosis (zones 1, 2 and 3 of liver acinus), presence of inflammatory infiltrate and granulomas in the liver parenchyma. High metabolic stress in the three zones and glycogen condensation, with the loss of histological architecture, positioning in grade 6 of NASH. Conclusions A high sucrose diet contributed to develop NAFLD in mice of the C57bl/6n strain. MSG showed light to moderate degree of NAFLD, whereas FSG showed a moderate to a high degree of NAFLD (steatosis and NASH) related to sucrose consumption. Funding Sources This work was supported by the Universidad Autónoma de Sinaloa.

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Effects of high sucrose diet, gemfibrozil, and their combination on plasma paraoxonase 1 activity and lipid levels in rats.

Acta Biochimica Polonica ◽

10.18388/abp.2010_2411 ◽

2010 ◽

Vol 57 (3) ◽

Cited By ~ 8

Author(s):

Marija Macan ◽

Nada Vrkić ◽

Ana Lucić Vrdoljak ◽

Božica Radić ◽

Vlasta Bradamante

Keyword(s):

Control Diet ◽

Paraoxonase 1 ◽

Pon1 Activity ◽

Control Group ◽

Lipid Levels ◽

Sucrose Diet ◽

High Sucrose Diet ◽

The Relationship ◽

High Sucrose ◽

Serum Pon1 Activity

We investigated the influence of high sucrose diet (HSD) after 3 or 5 weeks of administration on paraoxonase 1 (PON1) activity in plasma of normolipidemic rats and the relationship between serum PON1 activity, triacylglycerides (TGs), HDL and total cholesterol vs. the control group of rats fed normal, control diet (CD). Because the data about the influence of gemfibrozil (GEM) on PON1 activity are controversial, we also investigated its effects (administration in the 4th and 5th week in rats on HSD and CD) on plasma PON1 activity and lipid levels in normolipidemic rats, and in rats with hypertriglyceridemia caused by HSD. Our results obtained in rats on HSD show a significant increase of plasma TGs levels by 47% (P

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Role of the Mitochondrial Pyruvate Carrier in the Occurrence of Metabolic Inflexibility in Drosophila melanogaster Exposed to Dietary Sucrose

Metabolites ◽

10.3390/metabo10100411 ◽

2020 ◽

Vol 10 (10) ◽

pp. 411 ◽

Cited By ~ 1

Author(s):

Chloé J. Simard ◽

Mohamed Touaibia ◽

Eric Pierre Allain ◽

Etienne Hebert-Chatelain ◽

Nicolas Pichaud

Keyword(s):

Mitochondrial Respiration ◽

Standard Diet ◽

Dietary Carbohydrates ◽

Respiration Rates ◽

Mitochondrial Pyruvate Carrier ◽

Sucrose Diet ◽

High Sucrose Diet ◽

Metabolic Inflexibility ◽

High Sucrose

Excess dietary carbohydrates are linked to dysregulation of metabolic pathways converging to mitochondria and metabolic inflexibility. Here, we determined the role of the mitochondrial pyruvate carrier (MPC) in the occurrence of this metabolic inflexibility in wild-type (WT) and MPC1-deficient (MPC1def) flies that were exposed to diets with different sucrose concentrations for 15–25 days (Standard Diet: SD, Medium-Sucrose Diet: MSD, and High-Sucrose Diet: HSD). Our results showed that MPC1def flies had lower mitochondrial respiration rates than WT flies on the SD and MSD. However, when exposed to the HSD, WT flies displayed decreased mitochondrial respiration rates compared to MPC1def flies. WT flies exposed to the HSD also displayed increased proline contribution and slightly decreased MPC1 expression. Surprisingly, when fed the MSD and the HSD, few metabolites were altered in WT flies whereas MPC1def flies display significant accumulation of glycogen, glucose, fructose, lactate, and glycerol. Overall, this suggests that metabolic inflexibility starts to occur in WT flies after 15–25 days of exposure to the HSD whereas the MPC1def flies display metabolic inflexibility independently of the diet provided. This study thus highlights the involvement of MPC as an essential protein in Drosophila to maintain proper metabolic homeostasis during changes in dietary resources.

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Reduced reticulum–mitochondria Ca2+ transfer is an early and reversible trigger of mitochondrial dysfunctions in diabetic cardiomyopathy

Basic Research in Cardiology ◽

10.1007/s00395-020-00835-7 ◽

2020 ◽

Vol 115 (6) ◽

Author(s):

Maya Dia ◽

Ludovic Gomez ◽

Helene Thibault ◽

Nolwenn Tessier ◽

Christelle Leon ◽

...

Keyword(s):

Cardiac Function ◽

Diabetic Cardiomyopathy ◽

Standard Diet ◽

Mitochondrial Bioenergetics ◽

Mitochondrial Dysfunctions ◽

High Sucrose Diet ◽

High Sucrose ◽

Normal Cardiac Function

AbstractType 2 diabetic cardiomyopathy features Ca2+ signaling abnormalities, notably an altered mitochondrial Ca2+ handling. We here aimed to study if it might be due to a dysregulation of either the whole Ca2+ homeostasis, the reticulum–mitochondrial Ca2+ coupling, and/or the mitochondrial Ca2+ entry through the uniporter. Following a 16-week high-fat high-sucrose diet (HFHSD), mice developed cardiac insulin resistance, fibrosis, hypertrophy, lipid accumulation, and diastolic dysfunction when compared to standard diet. Ultrastructural and proteomic analyses of cardiac reticulum–mitochondria interface revealed tighter interactions not compatible with Ca2+ transport in HFHSD cardiomyocytes. Intramyocardial adenoviral injections of Ca2+ sensors were performed to measure Ca2+ fluxes in freshly isolated adult cardiomyocytes and to analyze the direct effects of in vivo type 2 diabetes on cardiomyocyte function. HFHSD resulted in a decreased IP3R–VDAC interaction and a reduced IP3-stimulated Ca2+ transfer to mitochondria, with no changes in reticular Ca2+ level, cytosolic Ca2+ transients, and mitochondrial Ca2+ uniporter function. Disruption of organelle Ca2+ exchange was associated with decreased mitochondrial bioenergetics and reduced cell contraction, which was rescued by an adenovirus-mediated expression of a reticulum-mitochondria linker. An 8-week diet reversal was able to restore cardiac insulin signaling, Ca2+ transfer, and cardiac function in HFHSD mice. Therefore, our study demonstrates that the reticulum–mitochondria Ca2+ miscoupling may play an early and reversible role in the development of diabetic cardiomyopathy by disrupting primarily the mitochondrial bioenergetics. A diet reversal, by counteracting the MAM-induced mitochondrial Ca2+ dysfunction, might contribute to restore normal cardiac function and prevent the exacerbation of diabetic cardiomyopathy.

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A binge high sucrose diet provokes systemic and cerebral inflammation in rats without inducing obesity

Scientific Reports ◽

10.1038/s41598-021-90817-z ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Omkar L. Patkar ◽

Abdalla Z. Mohamed ◽

Ashwin Narayanan ◽

Karine Mardon ◽

Gary Cowin ◽

...

Keyword(s):

Weight Gain ◽

Western Diet ◽

Control Group ◽

Slight Reduction ◽

Low Grade ◽

Cell Counts ◽

Sucrose Diet ◽

Normal Chow ◽

High Sucrose Diet ◽

High Sucrose

AbstractWhile the dire cardiometabolic consequences of the hypercaloric modern ‘Western’ diet are well known, there is not much information on the health impact of a high sucrose diet not inducing weight gain. Here, we tested the hypothesis that rats reared with intermittent binge access to sucrose in addition to normal chow would develop an inflammatory response in brain. To test this hypothesis, we undertook serial PET/MRI scans with the TSPO ligand [18F]DPA714 in a group of (n=9) rats at baseline and again after voluntarily consuming 5% sucrose solution three days a week for three months. Compared to a control group fed with normal chow (n=9), the sucrose rats indeed showed widespread increases in the availability of cerebral binding sites for the microglial marker, despite normal weight gain compared to the control diet group. Subsequent immunofluorescence staining of the brains confirmed the PET findings, showing a widespread 20% increase in the abundance of IBA-1-positive microglia with characteristic ‘semi-activated’ morphology in the binge sucrose rats, which had 23% lower density of microglial endpoints and 25% lower mean process length compared to microglia in the control rats with ordinary feeding. GFAP immunofluorescence showed no difference in astroglial coverage in the sucrose rats, except for a slight reduction in hypothalamus. The binge sucrose diet-induced neuroinflammation was associated with a significant elevation of white blood cell counts. Taking these results together, we find that long-term intake of sucrose in a binge paradigm, similar in sucrose content to the contemporary Western diet, triggered a low-grade systemic and central inflammation in non-obese rats. The molecular mechanism of this phenomenon remains to be established.

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Involvement of AMP-activated protein kinase in beneficial effects of betaine on high-sucrose diet-induced hepatic steatosis

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00133.2007 ◽

2007 ◽

Vol 293 (4) ◽

pp. G894-G902 ◽

Cited By ~ 76

Author(s):

Zhenyuan Song ◽

Ion Deaciuc ◽

Zhanxiang Zhou ◽

Ming Song ◽

Theresa Chen ◽

...

Keyword(s):

Protein Kinase ◽

Hepatic Steatosis ◽

Critical Role ◽

Standard Diet ◽

Fat Accumulation ◽

Beneficial Effects ◽

Sucrose Diet ◽

High Sucrose Diet ◽

Amp Activated Protein Kinase ◽

High Sucrose

Although simple steatosis was originally thought to be a pathologically inert histological change, fat accumulation in the liver may play a critical role not only in disease initiation, but also in the progression to nonalcoholic steatohepatitis and cirrhosis. Therefore, prevention of fat accumulation in the liver may be an effective therapy for multiple stages of nonalcoholic fatty liver disease (NAFLD). Promising beneficial effects of betaine supplementation on human NAFLD have been reported in some pilot clinical studies; however, data related to betaine therapy in NAFLD are limited. In this study, we examined the effects of betaine on fat accumulation in the liver induced by high-sucrose diet and evaluated mechanisms by which betaine could attenuate or prevent hepatic steatosis in this model. Male C57BL/6 mice weighing 20 ± 0.5 g (means ± SE) were divided into four groups (8 mice per group) and started on one of four treatments: standard diet (SD), SD+betaine, high-sucrose diet (HS), and HS + betaine. Betaine was supplemented in the drinking water at a concentration of 1% (wt/vol) (anhydrous). Long-term feeding of high-sucrose diet to mice caused significant hepatic steatosis accompanied by markedly increased lipogenic activity. Betaine significantly attenuated hepatic steatosis in this animal model, and this change was associated with increased activation of hepatic AMP-activated protein kinase (AMPK) and attenuated lipogenic capability (enzyme activities and gene expression) in the liver. Our findings are the first to suggest that betaine might serve as a therapeutic tool to attenuate hepatic steatosis by targeting the hepatic AMPK system.

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SHR-Zbtb16 Minimal Congenic Strain Reveals Nutrigenetic Interaction Between Zbtb16 and High-Sucrose Diet

Physiological Research ◽

10.33549/physiolres.934423 ◽

2020 ◽

pp. 521-527

Author(s):

E ŠKOLNÍKOVÁ ◽

L ŠEDOVÁ ◽

F LIŠKA ◽

O ŠEDA

Keyword(s):

Metabolic Syndrome ◽

Congenic Strain ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Metabolic Effects ◽

Standard Diet ◽

Low Density ◽

Sucrose Diet ◽

High Sucrose Diet ◽

High Sucrose

Both prenatal and postnatal excessive consumption of dietary sucrose or fructose was shown to be detrimental to health and contributing to pathogenesis of metabolic syndrome. Our knowledge of genetic determinants of individual sensitivity to sucrose-driven metabolic effects is limited. In this study, we have tested the hypothesis that a variation of metabolic syndrome-related gene, Zbtb16 (Zinc Finger and BTB Domain Containing 16 will affect the reaction to high-sucrose diet (HSD) content in “matched” nutritional exposition settings, i.e. maternal HSD with re-exposition to HSD in adulthood vs. standard diet. We compared metabolic profiles of adult males of spontaneously hypertensive rats (SHR) and a single-gene, minimal congenic strain SHR-Zbtb16 fed either standard diet or exposed to HSD prenatally throughout gestation and nursing and again at the age of 6 months for the period of 14 days. HSD exposition led to increased adiposity in both strains and decrease of glucose tolerance and cholesterol (Ch) concentrations in majority of low-density lipoprotein (LDL) particle classes and in very large and large high-density lipoprotein (HDL) in SHR-Zbtb16 male offspring. There was a similar pattern of HSD-induced increase of triacylglycerols in chylomicrons and very low-density lipoprotein (VLDL) of both strains, though the increase of (triacylglycerol) TAG content was clearly more pronounced in SHR. We observed significant STRAIN*DIET interactions for the smallest LDL particles as their TAG content decreased in SHR-Zbtb16 and did not change in SHR in response to HSD. In summary, we provide evidence of nutrigenetic interaction between Zbtb16 and HSD in context of pathogenesis of metabolic syndrome.

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Grandmother’s Diet Matters: Early Life Programming with Sucrose Influences Metabolic and Lipid Parameters in Second Generation of Rats

Nutrients ◽

10.3390/nu12030846 ◽

2020 ◽

Vol 12 (3) ◽

pp. 846 ◽

Cited By ~ 1

Author(s):

Elena Školníková ◽

Lucie Šedová ◽

Ondřej Šeda

Keyword(s):

Early Life ◽

Second Generation ◽

Hdl Cholesterol ◽

Female Offspring ◽

Standard Diet ◽

Increased Risk ◽

Sucrose Diet ◽

Fasting Glycaemia ◽

High Sucrose Diet ◽

High Sucrose

Early life exposure to certain environmental stimuli is related to the development of alternative phenotypes in mammals. A number of these phenotypes are related to an increased risk of disease later in life, creating a massive healthcare burden. With recent focus on the determination of underlying causes of common metabolic disorders, parental nutrition is of great interest, mainly due to a global shift towards a Western-type diet. Recent studies focusing on the increase of food or macronutrient intake don’t always consider the source of these nutrients as an important factor. In our study, we concentrate on the effects of high-sucrose diet, which provides carbohydrates in form of sucrose as opposed to starch in standard diet, fed in pregnancy and lactation in two subsequent generations of spontaneously hypertensive rats (SHR) and congenic SHR-Zbtb16 rats. Maternal sucrose intake increased fasting glycaemia in SHR female offspring in adulthood and increased their chow consumption in gravidity. High-sucrose diet fed to the maternal grandmother increased brown fat weight and HDL cholesterol levels in adult male offspring of both strains, i.e., the grandsons. Fasting glycaemia was however decreased only in SHR offspring. In conclusion, we show the second-generation effects of maternal exposition to a high-sucrose diet, some modulated to a certain extent by variation in the Zbtb16 gene.

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Comparing the Mathematics Continuous Performance Test With Other Measures of Tests of Attention

European Journal of Psychological Assessment ◽

10.1027/1015-5759/a000261 ◽

2016 ◽

Vol 32 (4) ◽

pp. 291-297 ◽

Cited By ~ 1

Author(s):

Dubi Lufi ◽

Shachar Pan

Keyword(s):

Performance Test ◽

Continuous Performance Test ◽

Clinical Population ◽

Control Group ◽

Continuous Performance ◽

Adhd Assessment ◽

Research Reporting ◽

Hyperactivity Disorder ◽

Continuous Performance Tests ◽

Better Than

Abstract. Several studies have shown that Continuous Performance Tests (CPT) can diagnose Attention Deficit Hyperactivity Disorder (ADHD) better than other tests. Research reporting comparisons of two or more CPT-type tests is scarce. The purpose of the study was to compare the Mathematics Continuous Performance Test (MATH-CPT) with another CPT-type test (CPT II) and a questionnaire (the Brown Scale). The comparison was carried out by looking at correlations among subscales and checking the precision of detecting ADHD. Ninety-five high school and college students participated in the study, 41 with ADHD were the research group and 54 were the control group. The participants performed the two tests and answered the questionnaire. The results showed that the MATH-CPT correctly identified 74.50% of the participants of both groups as compared to the 71.60% of the CPT II. Correlations between the two CPT-type tests were moderate; however, they were similar to correlations found in other studies comparing similar tools. The MATH-CPT, final attention formula, showed significant correlations with the Brown scales, while the CPT II, confidence index associated with ADHD assessment, showed nonsignificant correlations with the questionnaire. The study indicated that MATH-CPT can be used with a clinical population of ADHD and for research purposes.

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