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

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.

Download Full-text

Mechanical adaptations of skinned cardiac muscle in response to dietary-induced obesity during adolescence in rats

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2019-0726 ◽

2020 ◽

Vol 45 (8) ◽

pp. 893-901 ◽

Cited By ~ 1

Author(s):

Kevin Boldt ◽

Graham MacDonald ◽

Venus Joumaa ◽

Walter Herzog

Keyword(s):

Childhood Obesity ◽

Cardiac Muscle ◽

Cardiac Disease ◽

Calcium Sensitivity ◽

High Fat ◽

Shortening Velocity ◽

Increased Risk ◽

Sucrose Diet ◽

High Sucrose Diet ◽

High Sucrose

Childhood obesity is a major risk factor for heart disease during adulthood, independent of adulthood behaviours. Therefore, it seems that childhood obesity leads to partly irreversible decrements in cardiac function. Little is known about how obesity during maturation affects the mechanical properties of the heart. The purpose of this study was to evaluate contractile properties in developing hearts from animals with dietary-induced obesity (high-fat high-sucrose diet). We hypothesized that obesity induced during adolescence results in decrements in cardiac contractile function. Three-week-old rats (n = 16) were randomized into control (chow) or dietary-induced obesity (high-fat high-sucrose diet) groups. Following 14 weeks on the diet, skinned cardiac trabeculae fibre bundle testing was performed to evaluate active and passive force, maximum shortening velocity, and calcium sensitivity. Rats in the high-fat high-sucrose diet group had significantly larger body mass and total body fat percentage. There were no differences in maximal active or passive properties of hearts between groups. Hearts from the high-fat high-sucrose diet rats had significantly slower maximum shortening velocities and lower calcium sensitivity than controls. Decreased shortening velocity and calcium sensitivity in hearts of obese animals may constitute increased risk of cardiac disease in adulthood. Novelty Cardiac muscle from animals exposed to an obesogenic diet during development had lower shortening velocity and calcium sensitivity than those from animals fed a chow diet. These alterations in mechanical function may be a mechanism for the increased risk of cardiac disease observed in adulthood.

Download Full-text

High‐Fat High‐Sucrose Diet Increases ACE2 Receptor Expression in Lung and Pancreatic Islets in SIV‐Infected Rhesus Macaques: Implications for Increased Risk for SARS‐CoV‐2 Infection

The FASEB Journal ◽

10.1096/fasebj.2021.35.s1.02861 ◽

2021 ◽

Vol 35 (S1) ◽

Author(s):

Danielle Levitt ◽

Elizabeth Delery ◽

Liz Simon ◽

Patricia Molina

Keyword(s):

Pancreatic Islets ◽

Rhesus Macaques ◽

Receptor Expression ◽

High Fat ◽

Increased Risk ◽

Sucrose Diet ◽

High Sucrose Diet ◽

High Sucrose

Download Full-text

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.

Download Full-text

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.

Download Full-text

The effect of early-life stress and chronic high-sucrose diet on metabolic outcomes in female rats

Stress ◽

10.3109/10253890.2015.1079617 ◽

2015 ◽

Vol 18 (5) ◽

pp. 524-537 ◽

Cited By ~ 8

Author(s):

Jayanthi Maniam ◽

Christopher P. Antoniadis ◽

Margaret J. Morris

Keyword(s):

Life Stress ◽

Early Life ◽

Early Life Stress ◽

Female Rats ◽

Metabolic Outcomes ◽

Sucrose Diet ◽

High Sucrose Diet ◽

High Sucrose

Download Full-text

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.

Download Full-text

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.

Download Full-text

Chemically Contaminated Eel Fed to Pregnant and Lactating Mouse Dams Causes Hyperactivity in Their Offspring

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831/a000288 ◽

2016 ◽

Vol 86 (1-2) ◽

pp. 36-47 ◽

Cited By ~ 2

Author(s):

Imen Dridi ◽

Nidhal Soualeh ◽

Torsten Bohn ◽

Rachid Soulimani ◽

Jaouad Bouayed

Keyword(s):

Open Field ◽

Early Life ◽

Home Cage ◽

Anguilla Anguilla ◽

Acetylcholinesterase Activity ◽

Female Offspring ◽

Significant Inhibition ◽

Standard Diet ◽

Early Life Exposure ◽

Cage Test

Abstract.This study examined whether perinatal exposure to polluted eels (Anguilla anguilla L.) induces changes in the locomotor activity of offspring mice across lifespan (post-natal days (PNDs) 47 – 329), using the open field and the home cage activity tests. Dams were exposed during gestation and lactation, through diets enriched in eels naturally contaminated with pollutants including PCBs. Analysis of the eel muscle focused on the six non-dioxin-like (NDL) indicator PCBs (Σ6 NDL-PCBs: 28, 52, 101, 138, 153 and 180). Four groups of dams (n = 10 per group) received either a standard diet without eels or eels (0.8 mg/kg/day) containing 85, 216, or 400 ng/kg/day of ϵ6 NDL-PCBs. The open field test showed that early-life exposure to polluted eels increased locomotion in female offspring of exposed dams but not in males, compared to controls. This hyperlocomotion appeared later in life, at PNDs 195 and 329 (up to 32 % increase, p < 0.05). In addition, overactivity was observed in the home cage test at PND 305: exposed offspring females showed a faster overall locomotion speed (3.6 – 4.2 cm/s) than controls (2.9 cm/s, p <0.05); again, males remained unaffected. Covered distances in the home cage test were only elevated significantly in offspring females exposed to highest PCB concentrations (3411 ± 590 cm vs. 1377 ± 114 cm, p < 0.001). These results suggest that early-life exposure to polluted eels containing dietary contaminants including PCBs caused late, persistent and gender-dependent neurobehavioral hyperactive effects in offspring mice. Furthermore, female hyperactivity was associated with a significant inhibition of acetylcholinesterase activity in the hippocampus and the prefrontal cortex.

Download Full-text