scholarly journals The effect of maternal and post-weaning low and high glycaemic index diets on glucose tolerance, fat deposition and hepatic function in rat offspring

2015 ◽  
Vol 7 (3) ◽  
pp. 320-329 ◽  
Author(s):  
J. Gugusheff ◽  
P. Sim ◽  
A. Kheng ◽  
S. Gentili ◽  
M. Al-Nussairawi ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Later Life ◽  
Hepatic Function ◽  
Female Offspring ◽  
Glycaemic Index ◽  
Visceral Adiposity ◽  
Beneficial Effects ◽  
Pregnancy And Lactation ◽  
Total Body ◽  
The Impact

Clinical studies have reported beneficial effects of a maternal low glycaemic index (GI) diet on pregnancy and neonatal outcomes, but the impact of the diet on the offspring in later life, and the mechanisms underlying these effects, remain unclear. In this study, Albino Wistar rats were fed either a low GI (n=14) or high GI (n=14) diet during pregnancy and lactation and their offspring weaned onto either the low or high GI diet. Low GI dams had better glucose tolerance (AUC[glucose], 1322±55 v. 1523±72 mmol min/l, P<0.05) and a lower proportion of visceral fat (19.0±2.9 v. 21.7±3.8% of total body fat, P<0.05) compared to high GI dams. Female offspring of low GI dams had lower visceral adiposity (0.45±0.03 v. 0.53±0.03% body weight, P<0.05) and higher glucose tolerance (AUC[glucose], 1243±29 v. 1351±39 mmol min/l, P<0.05) at weaning, as well as lower hepatic PI3K-p85 mRNA at 12 weeks of age. No differences in glucose tolerance or hepatic gene expression were observed in male offspring, but the male low GI offspring did have reduced hepatic lipid content at weaning. These findings suggest that consuming a low GI diet during pregnancy and lactation can improve glucose tolerance and reduce visceral adiposity in the female offspring at weaning, and may potentially produce long-term reductions in the hepatic lipogenic capacity of these offspring.

scholarly journals Maternal Diet Influences the Reinstatement of Cocaine-Seeking Behavior and the Expression of Melanocortin-4 Receptors in Female Offspring of Rats

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1462
Author(s):  
Dawid Gawliński ◽  
Kinga Gawlińska ◽  
Małgorzata Frankowska ◽  
Małgorzata Filip
Keyword(s):  
Maternal Diet ◽  
Dorsal Striatum ◽  
Brain Structures ◽  
Female Offspring ◽  
Self Administration ◽  
Cocaine Seeking ◽  
Seeking Behavior ◽  
Pregnancy And Lactation ◽  
The Impact ◽  
Cocaine Reward

Recent studies have emphasized the role of the maternal diet in the development of mental disorders in offspring. Substance use disorder is a major global health and economic burden. Therefore, the search for predisposing factors for the development of this disease can contribute to reducing the health and social damage associated with addiction. In this study, we focused on the impact of the maternal diet on changes in melanocortin-4 (MC-4) receptors as well as on behavioral changes related to cocaine addiction. Rat dams consumed a high-fat diet (HFD), high-sugar diet (HSD, rich in sucrose), or mixed diet (MD) during pregnancy and lactation. Using an intravenous cocaine self-administration model, the susceptibility of female offspring to cocaine reward and cocaine-seeking propensities was evaluated. In addition, the level of MC-4 receptors in the rat brain structures related to cocaine reward and relapse was assessed. Modified maternal diets did not affect cocaine self-administration in offspring. However, the maternal HSD enhanced cocaine-seeking behavior in female offspring. In addition, we observed that the maternal HSD and MD led to increased expression of MC-4 receptors in the nucleus accumbens, while increased MC-4 receptor levels in the dorsal striatum were observed after exposure to the maternal HSD and HFD. Taken together, it can be concluded that a maternal HSD is an important factor that triggers cocaine-seeking behavior in female offspring and the expression of MC-4 receptors.

scholarly journals DHA Supplementation of Obese Rats throughout Pregnancy and Lactation Modifies Milk Composition and Anxiety Behavior of Offspring

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4243
Author(s):  
Elena Zambrano ◽  
Guadalupe L. Rodríguez-González ◽  
Luis A. Reyes-Castro ◽  
Claudia J. Bautista ◽  
Diana C. Castro-Rodríguez ◽  
...  
Keyword(s):  
Female Offspring ◽  
Milk Composition ◽  
Chain Polyunsaturated Fatty Acid ◽  
Dependent Manner ◽  
Maternal Weight ◽  
Female Wistar Rats ◽  
Pregnancy And Lactation ◽  
Anxiety Behavior ◽  
Total Fat ◽  
Total Body

We investigated if supplementing obese mothers (MO) with docosahexaenoic acid (DHA) improves milk long-chain polyunsaturated fatty acid (LCPUFA) composition and offspring anxiety behavior. From weaning throughout pregnancy and lactation, female Wistar rats ate chow (C) or a high-fat diet (MO). One month before mating and through lactation, half the mothers received 400 mg DHA kg−1 d−1 orally (C+DHA or MO+DHA). Offspring ate C after weaning. Maternal weight, total body fat, milk hormones, and milk nutrient composition were determined. Pups’ milk nutrient intake was evaluated, and behavioral anxiety tests were conducted. MO exhibited increased weight and total fat, and higher milk corticosterone, leptin, linoleic, and arachidonic acid (AA) concentrations, and less DHA content. MO male and female offspring had higher ω-6/ ω-3 milk consumption ratios. In the elevated plus maze, female but not male MO offspring exhibited more anxiety. MO+DHA mothers exhibited lower weight, total fat, milk leptin, and AA concentrations, and enhanced milk DHA. MO+DHA offspring had a lower ω-6/ω-3 milk intake ratio and reduced anxiety vs. MO. DHA content was greater in C+DHA milk vs. C. Supplementing MO mothers with DHA improves milk composition, especially LCPUFA content and ω-6/ω-3 ratio reducing offspring anxiety in a sex-dependent manner.

scholarly journals Maternal undernutrition during critical windows of development results in differential and sex-specific effects on postnatal adiposity and related metabolic profiles in adult rat offspring

2011 ◽  
Vol 108 (2) ◽  
pp. 298-307 ◽  
Author(s):  
G. J. Howie ◽  
D. M. Sloboda ◽  
M. H. Vickers
Keyword(s):  
Maternal Nutrition ◽  
Later Life ◽  
Hepatic Function ◽  
Postnatal Growth ◽  
Standard Diet ◽  
Adult Rat ◽  
Maternal Undernutrition ◽  
Specific Effects ◽  
Metabolic Outcomes ◽  
Pregnancy And Lactation

It is well established that altered maternal nutrition may induce long-term metabolic consequences in offspring. However, the effects of maternal undernutrition during different developmental windows on sex-specific growth and metabolism in offspring are not well defined. We investigated the effect of moderate maternal undernutrition during pregnancy and/or lactation on postnatal growth and metabolic outcomes in offspring. Wistar rats were randomly assigned to one of four groups: (1) control (CONT) dams fed a standard diet throughout pregnancy and lactation; (2) dams undernourished to 50 % of CONT during pregnancy (UNP); (3) dams fed at 50 % of CONT throughout lactation (UNL); (4) dams fed at 50 % of CONT throughout pregnancy and lactation (UNPL). UNP and UNPL offspring were lighter at birth compared to CONT and UNL. UNL and UNPL offspring were growth restricted at weaning and remained smaller into adulthood. UNP males and females developed increased adiposity and hyperleptinaemia in adulthood compared to all other groups. Adiposity in UNL and UNPL males was similar to CONT offspring. In UNL and UNPL females, adiposity was lower than for CONT females. Markers of bone mass, lipid metabolism and hepatic function were altered in UNP offspring but were similar in UNL and UNPL offspring compared to CONT. Lack of catch-up growth during lactation in offspring of undernourished mothers prevented development of adiposity and related metabolic disorders in later life. These data highlight that the timing and duration of undernutrition during critical windows of development exert differential effects on postnatal outcomes in a sex-specific manner.

scholarly journals Gestational Diabetes Mellitus: The Impact of Carbohydrate Quality in Diet

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1549 ◽  
Author(s):  
Tiziana Filardi ◽  
Francesca Panimolle ◽  
Clara Crescioli ◽  
Andrea Lenzi ◽  
Susanna Morano
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Dietary Intervention ◽  
Clinical Care ◽  
Insulin Requirement ◽  
Glycaemic Index ◽  
Current Evidence ◽  
Beneficial Effects ◽  
The Impact

Gestational diabetes mellitus (GDM) is defined as “glucose intolerance that is first diagnosed during pregnancy”. Mothers with GDM and their infants may experience both short and long term complications. Dietary intervention is the first therapeutic strategy. If good glycaemic control is not achieved, insulin therapy is recommended. There is no consensus on which nutritional approach should be used in GDM. In the last few years, there has been growing evidence of the benefits of a low glycaemic index (LGI) diet on diabetes and cardiovascular disease. The effect of a LGI diet on GDM incidence has been investigated as well. Several studies observed a lower incidence of GDM in LGI diet arms, without adverse maternal and fetal outcomes. The main positive effect of the LGI diet was the reduction of 2-h post-prandial glucose (PPG). Several studies have also evaluated the effect of the LGI diet in GDM treatment. Overall, the LGI diet might have beneficial effects on certain outcomes, such as 2-h PPG, fasting plasma glucose and lipid profile in patients with GDM. Indeed, most studies observed a significant reduction in insulin requirement. Overall, according to current evidence, the LGI nutritional approach is safe and it might therefore be considered in clinical care for GDM.

scholarly journals Maternal Consumption of a Diet Rich in Maillard Reaction Products Accelerates Neurodevelopment in F1 and Sex-Dependently Affects Behavioral Phenotype in F2 Rat Offspring

Foods ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 168 ◽  
Author(s):  
Melinda Csongová ◽  
Emese Renczés ◽  
Veronika Šarayová ◽  
Lucia Mihalovičová ◽  
Jakub Janko ◽  
...  
Keyword(s):  
Early Development ◽  
Hind Limb ◽  
Dietary Exposure ◽  
Later Life ◽  
Female Offspring ◽  
Behavioral Phenotype ◽  
Control Group ◽  
Maillard Reaction Products ◽  
Reaction Products ◽  
Pregnancy And Lactation

Thermal processing of foods at temperatures > 100 °C introduces considerable amounts of advanced glycation end-products (AGEs) into the diet. Maternal dietary exposure might affect the offspring early development and behavioral phenotype in later life. In a rat model, we examined the influence of maternal (F0) dietary challenge with AGEs-rich diet (AGE-RD) during puberty, pregnancy and lactation on early development, a manifestation of physiological reflexes, and behavioral phenotype of F1 and F2 offspring. Mean postnatal day of auditory conduit and eye opening, or incisor eruption was not affected by F0 diet significantly. F1 AGE-RD offspring outperformed their control counterparts in hind limb placing, in grasp tests and surface righting; grandsons of AGE-RD dams outperformed their control counterparts in hind limb placing and granddaughters in surface righting. In a Morris water maze, female AGE-RD F1 and F2 offspring presented better working memory compared with a control group of female offspring. Furthermore, male F2 AGE-RD offspring manifested anxiolysis-like behavior in a light dark test. Mean grooming time in response to sucrose splash did not differ between dietary groups. Our findings indicate that long-term maternal intake of AGE-RD intergenerationally and sex-specifically affects development and behavioral traits of offspring which have never come into direct contact with AGE-RD.

scholarly journals Impact of Maternal Intake of Artificial Sweetener, Acesulfame-K, on Metabolic and Reproductive Health Outcomes in Male and Female Mouse Offspring

2021 ◽  
Vol 8 ◽  
Author(s):  
Pania E. Bridge-Comer ◽  
Mark H. Vickers ◽  
Jacob Morton-Jones ◽  
Ana Spada ◽  
Jing Rong ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Pregnant Women ◽  
Female Offspring ◽  
Male Offspring ◽  
Dietary Advice ◽  
Oral Glucose ◽  
Artificial Sweetener ◽  
Adipocyte Size ◽  
Gene Markers ◽  
The Impact

Guidelines advising pregnant women to avoid food and beverages with high fat and sugar have led to an increase in the consumption of “diet” options sweetened by artificial sweeteners (AS). Yet, there is limited information regarding the impact of AS intake during pregnancy on the long-term risk of cardiometabolic and reproductive complications in adult offspring. This study examined the influence of maternal acesulfame-K (Ace-K) and fructose consumption on metabolic and reproductive outcomes in offspring. Pregnant C57BL/6 mice received standard chow ad-libitum with either water (CD), fructose (Fr; 20% kcal intake), or AS (AS; 12.5 mM Ace-K) throughout pregnancy and lactation (n = 8/group). Postweaning offspring were maintained on a CD diet for the remainder of the experiment. Body weight, food intake, and water intake were measured weekly. Oral glucose tolerance tests (OGTT) were undertaken at 12 weeks, and the offspring were culled at week 14. Female, but not male, AS groups exhibited decreased glucose tolerance compared to Fr. There was an increase in gonadal fat adipocyte size in male offspring from AS and Fr groups compared to CD groups. In female offspring, adipocyte size was increased in the Fr group compared to the CD group. In female, but not male offspring, there was a trend toward increase in Fasn gene expression in AS group compared to the CD group. Maternal AS and Fr also negatively impacted upon female offspring estrus cycles and induced alterations to markers associated with ovulation. In summary, exposure to Ace-k via the maternal diet leads to impaired glucose tolerance and impacts adipocyte size in a sex-specific manner as well as significantly affecting estrus cycles and related gene markers in female offspring. This has implications in terms of providing tailored dietary advice for pregnant women and highlights the potential negative influence of artificial sweetener intake in the context of intergenerational impacts.

Maternal protein restriction leads to hyperinsulinemia and reduced insulin-signaling protein expression in 21-mo-old female rat offspring

2005 ◽  
Vol 288 (2) ◽  
pp. R368-R373 ◽  
Author(s):  
D. S. Fernandez-Twinn ◽  
A. Wayman ◽  
S. Ekizoglou ◽  
M. S. Martin ◽  
C. N. Hales ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Insulin Signaling ◽  
Plasma Insulin ◽  
Female Offspring ◽  
Protein Restriction ◽  
Female Rat ◽  
Pregnancy And Lactation

Human adult diseases such as cardiovascular disease, hypertension, and type 2 diabetes have been epidemiologically linked to poor fetal growth and development. Male offspring of rat dams fed a low-protein (LP) diet during pregnancy and lactation develop diabetes with concomitant alterations in their insulin-signaling mechanisms. Such associations have not been studied in female offspring. The aim of this study was to determine whether female LP offspring develop diabetes in later life. Control and LP female offspring groups were obtained from rat dams fed a control (20% protein) or an isocaloric (8% protein) diet, respectively, throughout pregnancy and lactation. Both groups were weaned and maintained on 20% normal laboratory chow until 21 mo of age when they underwent intravenous glucose tolerance testing (IVGTT). Fasting glucose was comparable between the two groups; however, LP fasting insulin was approximately twofold that of controls ( P < 0.02). Glucose tolerance during IVGTT was comparable between the two groups; however, LP peak plasma insulin at 4 min was approximately threefold higher than in controls ( P < 0.001). LP plasma insulin area under the curve was 1.9-fold higher than controls ( P < 0.02). In Western blots, both muscle protein kinase C-ζ expression and p110β-associated p85α in abdominal fat were reduced ( P < 0.05) in LPs. Hyperinsulinemia in response to glucose challenge coupled with attenuation of certain insulin-signaling molecules imply the development of insulin resistance in LP muscle and fat. These observations suggest that intrauterine protein restriction leads to insulin resistance in females in old age and, hence, an increased risk of type 2 diabetes.

scholarly journals Impact of overweight and glucose tolerance on postprandial responses to high- and low-glycaemic index meals

2011 ◽  
Vol 105 (11) ◽  
pp. 1627-1634 ◽  
Author(s):  
Mia-Maria Perälä ◽  
Katja A. Hätönen ◽  
Jarmo Virtamo ◽  
Johan G. Eriksson ◽  
Harri K. Sinkko ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Postprandial Glucose ◽  
Glycaemic Index ◽  
Normal Weight ◽  
Physiological Characteristics ◽  
Fasting State ◽  
Lower Glucose ◽  
Insulin Responses ◽  
The Impact ◽  
Overweight Subjects

The beneficial effects of a low-glycaemic index (GI) meal on postprandial glucose and insulin levels have been demonstrated. However, limited data are available on the impact of overweight and glucose tolerance on postprandial responses to different GI meals. Our aim was to study the effects of physiological characteristics on postprandial glucose, insulin and lipid responses and the relative glycaemic response (RGR) of a low-GI (LGI) and a high-GI (HGI) meal. We recruited twenty-four normal-weight and twenty-four overweight subjects, twelve with normal glucose tolerance (NGT) and twelve with impaired glucose tolerance (IGT) in each group. Both test meals were consumed once and the glucose reference twice. Blood glucose and insulin were measured in the fasting state and over a 2 h period after each study meal, and TAG and NEFA were measured in the fasting state and over a 5 h period. The glucose responses of subjects with IGT differed significantly from those of subjects with NGT. The highest insulin responses to both meals were observed in overweight subjects with IGT. Physiological characteristics did not influence TAG or NEFA responses or the RGR of the meals. The LGI meal resulted in lower glucose (P < 0·001) and insulin (P < 0·001) responses, but higher TAG responses (P < 0·001), compared with the HGI meal. The GI of the meals did not affect the NEFA responses. In conclusion, the LGI meal causes lower glucose and insulin responses, but higher TAG responses, than the HGI meal. The RGR of the meals does not differ between normal-weight and overweight subjects with NGT or IGT.

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