Hepatic Epigenetic Reprogramming After Liver Resection in Offspring Alleviates the Effects of Maternal Obesity.

Obesity has become a public health problem in recent decades, and during pregnancy, it can lead to an increased risk of gestational complications and permanent changes in the offspring resulting from a process known as metabolic programming. The offspring of obese dams are at increased risk of developing non-alcoholic fatty liver disease (NAFLD), even in the absence of high-fat diet consumption. NAFLD is a chronic fatty liver disease that can progress to extremely severe conditions that require surgical intervention with the removal of the injured tissue.

Effect of acute swimming exercise at different intensities but equal total load over metabolic and molecular responses in swimming rats.

Acute metabolic and molecular response to exercise may vary according to exercise's intensity and duration. However, there is a lack regarding specific tissue alterations after acute exercise with aerobic or anaerobic predominance. The present study investigated the effects of acute exercise performed at different intensities, but with equal total load on molecular and physiological responses in swimming rats.

Iron deficiency in pregnancy: Influence on sleep, behavior, and molecular markers of adult male offspring.

Iron restriction during pregnancy can lead to iron deficiency and changes in the dopaminergic system in the adulthood of offspring, and restless legs syndrome (RLS) is closely related to these changes. Objectives: Analyze whether iron restriction during pregnancy would cause changes in the behavior, sleep, and dopaminergic system of the male offspring. In addition, we aimed to assess whether exercise would be able to modulate these variables.

MicroRNA Let-7 targets AMPK and impairs hepatic lipid metabolism in offspring of maternal obese pregnancies.

Nutritional status during gestation may lead to a phenomenon known as metabolic programming, which can be triggered by epigenetic mechanisms. The Let-7 family of microRNAs were one of the first to be discovered, and are closely related to metabolic processes. Bioinformatic analysis revealed that Prkaa2, the gene that encodes AMPK α2, is a predicted target of Let-7.

Load-matched acute and chronic exercise induce changes in mitochondrial biogenesis and metabolic markers.

We investigated the effects of acute and chronic exercise, prescribed in different intensity zones, but with total load-matched on mitochondrial markers (cytochrome C oxidase subunit IV (COX-IV), mitochondrial transcription factor A (Tfam), and citrate synthase (CS) activity in skeletal muscles, heart, and liver), glycogen stores, aerobic capacity, and anaerobic index in swimming rats. For this, 2 experimental designs were performed (acute and chronic efforts). Load-matched exercises were prescribed below, above, and on the anaerobic threshold (AnT), determined by the lactate minimum test.

Acute effects of fatty acids on autophagy in NPY neurones.

High-fat diet (HFD) feeding is deleterious to hypothalamic tissue, leading to inflammation and lipotoxicity, as well as contributing to central insulin resistance. Autophagy is a process that restores cellular homeostasis by degrading malfunctioning organelles and proteins. Chronic HFD-feeding down-regulates hypothalamic autophagy.

Periodized versus non-periodized swimming training with equal total training load: Physiological, molecular and performance adaptations in Wistar rats.

This study investigated the effect of non-periodized training performed at 80, 100 and 120% of the anaerobic threshold intensity (AnT) and a linear periodized training model adapted for swimming rats on the gene expression of monocarboxylate transporters 1 and 4 (MCT1 and 4, in soleus and gastrocnemius muscles), protein contents, blood biomarkers, tissue glycogen, body mass, and aerobic and anaerobic capacities. Sixty Wistar rats were randomly divided into 6 groups (n = 10 per group): a baseline (BL; euthanized before training period), a control group (GC; not exercised during the training period), three groups exercised at intensities equivalent to 80, 100 and 120% of the AnT (G80, G100 and G120, respectively) at the equal workload and a linear periodized training group (GPE). Each training program lasted 12 weeks subdivided into three periods: basic mesocycle (6 weeks), specific mesocycle (5 weeks) and taper (1 week).

Modulation of hypothalamic S6K1 and S6K2 alters feeding behavior and systemic glucose metabolism.

The mTOR/S6Ks signaling is one of the intracellular pathways important for metabolic control, acting both peripherally and centrally. In the hypothalamus, mTOR/S6Ks axis mediates the action of leptin and insulin and can modulate the expression of neuropeptides. We analyzed the role of different S6Ks isoforms in the hypothalamic regulation of metabolism.

Lipid overload during gestation and lactation can independently alter lipid homeostasis in offspring and promote metabolic impairment after new challenge to high-fat diet.

Background: Nutritional status in early life is critically involved in the metabolic phenotype of offspring. However the changes triggered by maternal consumption of high-fat diet (HFD) in pre- or postnatal period should be better understood. Here we evaluated whether maternal HFD consumption during gestation and lactation could differently affect liver miR-122 and miR-370 expression leading to metabolic damages observed in offspring.

Lactate minimum underestimates the maximal lactate steady-state in swimming mice.

The intensity of lactate minimum (LM) has presented a good estimate of the intensity of maximal lactate steady-state (MLSS); however, this relationship has not yet been verified in the mouse model. We proposed validating the LM protocol for swimming mice by investigating the relationship among intensities of LM and MLSS as well as differences between sexes, in terms of aerobic capacity. Nineteen mice (male: 10, female: 9) were submitted to the evaluation protocols for LM and MLSS.

Diet-Induced Maternal Obesity Alters Insulin Signalling in Male Mice Offspring Rechallenged with a High-Fat Diet in Adulthood.

Modern lifestyle has resulted in an increase in the prevalence of obesity and its comorbidities in pregnant women and the young population. It has been well established that the consumption of a high-fat diet (HFD) has many direct effects on glucose metabolism. However, it is important to assess whether maternal consumption of a HFD during critical periods of development can lead to metabolic changes in the offspring metabolism.

Autophagy proteins are modulated in the liver and hypothalamus of the offspring of mice with diet-induced obesity.

Nutritional excess during pregnancy and lactation has a negative impact on offspring phenotype. In adulthood, obesity and lipid overload represent factors that compromise autophagy, a process of lysosomal degradation. Despite knowledge of the impact of obesity on autophagy, changes in offspring of obese dams have yet to be investigated.

High-fat diet during pregnancy and lactation impairs the cholinergic anti-inflammatory pathway in the liver and white adipose tissue of mouse offspring.

Cholinergic anti-inflammatory pathway (CAP) prevents inflammatory cytokines production. The main was to evaluate the effect of maternal obesity on cholinergic pathway in the offspring. Female mice were subjected to either standard chow (SC) or high-fat diet (HFD) during pregnancy and the lactation period.