Publications by authors named "Nadezhda Bazhan"

Article Synopsis
  • The study explored how the timing of starting an obesogenic diet (Cafeteria Diet) affects obesity traits in male and female mice, focusing on pre-puberty and post-puberty initiation.
  • Male mice that started the diet before puberty displayed better metabolic health with lower body weight and improved fat metabolism compared to those starting after puberty.
  • Conversely, female mice starting the diet before puberty showed poorer metabolic profiles, including higher triglycerides and lower insulin sensitivity, showcasing gender differences in diet impact on obesity development.
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  • FGF21 shows potential as a treatment for obesity, diabetes, and non-alcoholic fatty liver disease (NAFLD), but its effects vary between male and female mice with mutations impacting melanocortin receptors.
  • A study found that female mice had higher obesity rates and different metabolic responses compared to males after FGF21 treatment, indicating sex plays a role in how FGF21 affects metabolism.
  • While FGF21 increased food intake and activity in both sexes, it only improved metabolic issues like hyperinsulinemia and liver fat in male mice, suggesting the treatment's benefits are more significant for males.
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  • * Female mice showed a stronger preference for high-fat diets, less body fat, and more favorable blood parameters than males, indicating potential sex-based differences in obesity development.
  • * FGF21 treatment reduced fat accumulation and improved metabolic markers in both sexes, but it specifically induced beneficial gene expression changes in the female mice's white adipose tissue.
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Fasting is often used for obesity correction but the "refeeding syndrome" limits its efficiency, and molecular mechanisms underlying metabolic response to different food availability are under investigation. Sex was shown to affect hormonal and metabolic reactions to fasting/refeeding. The aim of this study was to evaluate hormonal and transcriptional responses to fasting and refeeding in male and female C57Bl/6J mice.

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Obesity during pregnancy has been shown to increase the risk of metabolic diseases in the offspring. However, the factors within the maternal milieu which affect offspring phenotypes and the underlying mechanisms remain unknown. The adipocyte hormone leptin plays a key role in regulating energy homeostasis and is known to participate in sex-specific developmental programming.

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C57Bl mice exhibit impaired glucose metabolism by the late adult age under standard living conditions. The aim of this study was to evaluate white adipose tissue (WAT), brown adipose tissue (BAT), and skeletal muscle expression of genes involved in carbohydrate-lipid metabolism at postpubertal stages preceding the late adult age in C57Bl mice. Muscle mRNA levels of uncoupling protein 3 () and carnitine palmitoyltransferase 1 () (indicators of FFA oxidation), WAT mRNA levels of hormone-sensitive lipase () and lipoprotein lipase () (indicators of lipolysis and lipogenesis), muscle and WAT mRNA levels of the type 4 glucose transporter (indicators of insulin-dependent glucose uptake), and BAT mRNA levels of uncoupling protein 1 () (indicator of thermogenesis) were measured in fed and 16 h-fasted mice in three age groups: 10-week-old (young), 15-week-old (early adult), and 30-week-old (late adult).

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Maternal obesity increases the risk of obesity in offspring, and obesity is accompanied by an increase in blood leptin levels. The "yellow" mutation at the mouse agouti locus (A(y)) increases blood leptin levels in C57BL preobese pregnant mice without affecting other metabolic characteristics. We investigated the influence of the A(y) mutation or leptin injection at the end of pregnancy in C57BL mice on metabolic phenotypes and the susceptibility to diet-induced obesity (DIO) in offspring.

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The prevalence of obesity is increasing worldwide with serious consequences such as diabetes mellitus type 2 and cardiovascular diseases. Emotional stress is considered to be one of the main reasons of obesity development in humans. However, there are some contradictory results, which should be addressed.

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Objective: The antagonism of Agouti protein (AP) and Agouti-related protein on melanocortin receptors suggests an inhibitory role in the regulation of steroidogenesis. However, we have previously demonstrated that ectopic AP overexpression increased restraint-induced corticosterone release and adrenal reactivity to ACTH in mice. A high steroidogenic response to ACTH may be a consequence of a stimulatory AP action on the adenylate cyclase (AC) and/or intracellular steroidogenic enzymes.

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Article Synopsis
  • Agouti protein (AP) and agouti-related protein act as antagonists to melanocortin receptors, impacting the hypothalamo-pituitary-adrenal (HPA) axis and are involved in obesity profiles seen in agouti yellow (A(y)) mice.
  • The study compared HPA function in two groups of 3-month-old male C57Bl/6J mice with differing agouti genotypes (A(y)/a and a/a) using various stress stimuli to assess HPA response.
  • Results indicated that AP overexpression enhances HPA axis responses to stress independent of obesity; A(y)/a mice showed greater adrenal responsiveness to ACTH and improved stress-induced feedback inhibition with dexamethasone compared to a/a mice
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