Vitamin D deficiency aggravates the liver metabolism and inflammation in ovariectomized mice.

Aims: A prevalence of vitamin D deficiency has been reported in association with the postmenopause. Thus, we aimed to experimentally study the effect of the vitamin D deficiency and ovariectomy, alone or combined, in the liver damage.

Main Methods: Three-months-old female mice C57BL/6 with bilateral ovariectomy (Ovx group, n = 30) or a sham procedure (n = 30) were separated feeding control diet (C, n = 15) or a diet restricted in vitamin D (D-, n = 15) during additional 12 weeks.

Vitamin D Deficiency Increases Lipogenesis and Reduces Beta-Oxidation in the Liver of Diet-Induced Obese Mice.

The study was conducted to understand better the mechanisms involved in liver changes when there is a combination of diet-induced obesity (DIO) and vitamin D deficiency (VDD). After 8 wk of feeding a control diet (C group) or a high-fat diet (HF), both with vitamin D, and counterpart groups without vitamin D (VitD- groups), we found in plasma: higher alanine aminotransferase, and aspartate aminotransferase in the VitD- groups, and more elevated total cholesterol in the HF group. Compared to their counterparts, HF and HF/VitD- showed hyperinsulinemia and higher hepatic triglycerides and steatosis.

Differential actions of PPAR-α and PPAR-β/δ on beige adipocyte formation: A study in the subcutaneous white adipose tissue of obese male mice.

Background And Aims: Obesity compromises adipocyte physiology. PPARs are essential to adipocyte plasticity, but its isolated role in the browning phenomenon is not clear. This study aimed to examine whether activation of PPAR-α or PPAR-β/δ could induce beige cell depots in the subcutaneous white adipose tissue of diet-induced obese mice.

Father's obesity programs the adipose tissue in the offspring via the local renin-angiotensin system and MAPKs pathways, especially in adult male mice.

Purpose: Studies demonstrated the influence of mother's obesity on offspring. However, the father is also related to programming the future generation. The study aimed to evaluate the effects of father's obesity upon white adipose tissue (WAT) remodeling, resulting in activation of signaling pathways and inflammation in male and female offspring.

The insulin-signaling pathway of the pancreatic islet is impaired in adult mice offspring of mothers fed a high-fat diet.

Objective: Mothers fed a high-fat (HF) diet can cause different adverse alterations in their offspring. The study aimed to verify the pancreatic islet structure and insulin-signaling pathway in adulthood of offspring of mothers fed a HF diet during the pregnancy.

Methods: Female mice (mothers) were randomly assigned to receive either standard chow (Mo-SC) or a HF diet (Mo-HF) ad libitum.

Adverse effects of vitamin D deficiency on the Pi3k/Akt pathway and pancreatic islet morphology in diet-induced obese mice.

Scope: To investigate the impact of vitamin D deficiency on insulin resistance and abnormal glucose homeostasis in obesity.

Methods And Results: Sixty male C57BL/6 mice (3 months old) were fed a control diet (C-10% energy as fat) or a high-fat diet (HF-50% energy as fat), with or without vitamin D, for 8 weeks. There was no difference in body mass between the HF and HF/VitD- groups.

High-intensity interval training beneficial effects on body mass, blood pressure, and oxidative stress in diet-induced obesity in ovariectomized mice.

Aims: To investigate the possible beneficial effect of high-intensity interval training (HIIT) on skeletal muscle oxidative stress, body mass (BM) and systolic blood pressure (SBP) in ovariectomized mice fed or not fed a high-fat diet.

Main Methods: Three-month-old female C57BL/6 mice were bilaterally ovariectomized (OVX group) or submitted to surgical stress without ovariectomy (SHAM group) and separated into standard chow (SHAM-SC; OVX-SC) and high-fat diet (SHAM-HF; OVX-HF) groups. After 13 weeks, an HIIT program (swimming) was carried out for 8 weeks in non-trained (NT) and trained (T) groups.

PPAR-α agonist elicits metabolically active brown adipocytes and weight loss in diet-induced obese mice.

Obesity is considered a public health problem worldwide. Fenofibrate, a selective peroxisome proliferator-activated receptor α (PPAR-α) agonist, elicits weight loss in animal models. This study aimed to examine the effects of fenofibrate on energy expenditure, body mass (BM) and gene expression of thermogenic factors in brown adipose tissue of diet-induced obese mice.

Early hepatic insult in the offspring of obese maternal mice.

We hypothesized that the maternal obesity initiates metabolic disorders associated with oxidative stress in the liver of offspring since early life. Mouse's mothers were assigned into 2 groups according to the diet offered (n = 10 per group): standard chow (SC) or high-fat diet (HF). The results revealed that HF offspring had an increase in body mass at day 10 (+25%, P < .

Fenofibrate (PPARalpha agonist) induces beige cell formation in subcutaneous white adipose tissue from diet-induced male obese mice.

Browning is characterized by the formation of beige/brite fat depots in subcutaneous white adipose tissue (sWAT). This study aimed to examine whether the chronic activation of PPARalpha by fenofibrate could induce beige cell depots in the sWAT of diet-induced obese mice. High-fat fed animals presented overweight, insulin resistance and displayed adverse sWAT remodeling.

Maternal obesity during the preconception and early life periods alters pancreatic development in early and adult life in male mouse offspring.

Maternal obesity induced by a high fat (HF) diet may program susceptibility in offspring, altering pancreatic development and causing later development of chronic degenerative diseases, such as obesity and diabetes. Female mice were fed standard chow (SC) or an HF diet for 8 weeks prior to mating and during the gestational and lactational periods. The male offspring were assessed at birth, at 10 days, and at 3 months of age.

An early fish oil-enriched diet reverses biochemical, liver and adipose tissue alterations in male offspring from maternal protein restriction in mice.

Fetal programming is linked to adulthood metabolic and chronic diseases. We hypothesized that early fish oil (FO) intake would revert the programming responses in adult offspring. Pregnant mice were fed either standard chow (SC) or a low-protein diet (LP) throughout pregnancy/lactation.