Palm and interesterified palm oil-enhanced brown fat whitening contributes to metabolic dysfunction in C57BL/6J mice.

Palm oil is widely used in the food industry owing to its high stability and versatility. The interesterified version has been used as an alternative to oils rich in trans fatty acids. However, the health effects of these vegetable oils are not yet fully understood.

Metabolic consequences of interesterified palm oil and PCB-126 co-exposure in C57BL/6 mice.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is defined as morphofunctional changes in the liver. Studies have shown that Westernized eating patterns and environmental pollutants can directly induce the development of MASLD. This study evaluates the effect of co-exposure to interesterified palm oil (IPO) and 3,3',4,4',5-pentachlorobiphenyl (PCB-126) on the progression of MASLD in an animal model.

Long-term exposure to polychlorinated biphenyl 126 induces liver fibrosis and upregulates miR-155 and miR-34a in C57BL/6 mice.

Environmental pollutants, including polychlorinated biphenyls (PCBs), act as endocrine disruptors and impair various physiological processes. PCB 126 is associated with steatohepatitis, fibrosis, cirrhosis, and other hepatic injuries. These disorders can be regulated by microRNAs (miRNAs).

L. and synephrine improve brown adipose tissue function in adolescent mice programmed by early postnatal overfeeding.

Introduction And Aims: Obesity is a multifactorial condition with high health risk, associated with important chronic disorders such as diabetes, dyslipidemia, and cardiovascular dysfunction. L. () is a medicinal plant, and its active component, synephrine, a β-3 adrenergic agonist, can be used for weight loss.

Phenolic-rich smoothie consumption ameliorates non-alcoholic fatty liver disease in obesity mice by increasing antioxidant response.

Consumption of foods rich in phenolic compounds can be beneficial for health. This study aimed to examine whether the consumption of a phenolic-rich smoothie, based on juçara, strawberry and banana, ameliorates metabolic status and liver damage of diet-induced obese mice. Forty male C57BL/6J mice were assigned into four groups (n = 10) and fed control diet with free access to water (C) or phenolic-rich smoothie (C-S), or fed high-fat diet with free access to water (HF) or phenolic-rich smoothie (HF-S) for five weeks.

Early life nicotine exposure alters mRNA and microRNA expressions related to thyroid function and lipid metabolism in liver and BAT of adult wistar rats.

In rats, maternal nicotine exposure during lactation induces obesity, thyroid dysfunction, brown adipose tissue (BAT) hypofunction and liver alterations in adult offspring. Both thyroid function and lipid metabolism are influenced by gene silencing mediated by microRNAs (miRNAs). Here we investigated long-term effects of early nicotine exposure on molecular and epigenetic mechanisms closely related to thyroid and lipid metabolism, through the expression of mRNAs and miRNAs in BAT and liver of adult male and female offspring.

Maternal coconut oil intake on lactation programs for endocannabinoid system dysfunction in adult offspring.

Maternal exposure to coconut oil metabolically programs adult offspring for overweight, hyperphagia and hyperleptinemia. We studied the neuroendocrine mechanisms by which coconut oil supplementation during breastfeeding as well as continued exposure of this oil throughout life affect the feeding behavior of the progeny. At birth, pups were divided into two groups: Soybean oil (SO) and Coconut oil (CO).

Bromocriptine treatment at the end of lactation prevents hyperphagia, higher visceral fat and liver triglycerides in early-weaned rats at adulthood.

Non-pharmacological early weaning (NPEW) leads offspring to obesity, higher liver oxidative stress and microsteatosis in adulthood. Pharmacological EW (PEW) by maternal treatment with bromocriptine (BRO) causes obesity in the adult progeny but precludes hepatic injury. To test the hypothesis that BRO prevents the deleterious changes of NPEW, we injected BRO into the pups from the NPEW model in late lactation.

Dietary calcium supplementation in adult rats reverts brown adipose tissue dysfunction programmed by postnatal early overfeeding.

Brown adipose tissue (BAT) dysfunction is associated with obesity and its comorbidities, such as hypertension, and the improvement of BAT function seems important for obesity management. Here we investigated the effects of dietary calcium supplementation on BAT autonomic nerve activity, sympathoadrenal function and cardiovascular parameters in adult obese rats that were raised in small litters (SL group). Three days after birth, SL litters were adjusted to three pups to induce early overfeeding.