Leptin

The escalating global obesity epidemic underscores the need to understand its intricate health implications. Research highlights associations between elevated body mass index (BMI) and structural changes in both white and gray matter (WM, GM). Given the indirect nature of BMI as an indicator of adiposity, a comprehensive evaluation of body composition becomes essential. This study explores distinct adipose tissue compartments, adipokine levels, and their interplay with structural alterations in both WM and GM, elucidating the complex relationship between obesity, brain structure, and metabolic

Recently, a central role of butyrylcholinesterase (BChE) in pathogenesis of obesity has been proposed. As BChE was shown to inactivate a hunger hormone, ghrelin, it has been suggested to control appetite and glucose metabolism by regulating ghrelin signaling in hypothalamus. The aim of our study was therefore to investigate the relationship between obesity induced by high-fat/high-fructose diet and BChE activity. We studied impact of the diet-induced obesity on serum BChE and vise-versa an effect of BChE inhibition on obesity development. Adults male Wistar rats were fed with standard or high-

Nutrient composition in obesogenic diets may influence the severity of disorders associated with obesity such as insulin-resistance and chronic inflammation. Here we hypothesized that obesogenic diets rich in fat and varying in fatty acid composition, particularly in omega 6 (ω6) to omega 3 (ω3) ratio, have various effects on energy metabolism, neuroinflammation and behavior. Mice were fed either a control diet or a high fat diet (HFD) containing either low (LO), medium (ME) or high (HI) ω6/ω3 ratio. Mice from the HFD-LO group consumed less calories and exhibited less body weight gain compared

Obesity, a widespread health issue, accompanied by various metabolism-related disabilities, has emerged as a significant public health challenge. Primary intervention for obesity involves lifestyle changes, including dietary treatments. The ketogenic diet (KD) is increasingly recognized as a potential remedy for obesity, with its efficacy attributed to appetite suppression in the hypothalamus.The study aimed to evaluate how the metabolic changes in hypothalamus, associated with obesity affect the mechanisms responsible for appetite regulation during KD treatment.Adult male mice were subjected

…Leptin is an adipokine that exerts neurotrophic effects in the hippocampus, promoting synaptogenesis and synaptic plasticity. Meanwhile, rodents with altered leptin signaling exhibit impairments in these processes and defects in hippocampal-related functions. Leptin increases mushroom spines and the frequency of mini excitatory postsynaptic currents (mEPSCs) in developing hippocampal neurons, evidencing increased functional glutamatergic synapses. Given the presu

…anorexigenic effects of the adipokine leptin (Lep), as well as to promote adipose tissue (AT) lipolysis at the periphery. Here, we sought to address whether Oxt neurons could directly respond to Lep, and if any such regulatory cascade would increase Oxt levels in plasma. Adult C57BL/6 mice were intraperitoneally injected with mouse recombinant leptin (0.5 mg/kg) or saline, while others were subjected to standard or high-fat diet (HFD). Hypothalamus, AT

…loss of fat mass results in hypoleptinemia, which initiates multiple starvation-related adaptive functions. Although leptin administration showed beneficial effects in treatment of symptoms of anorexia nervosa, including anxiety, neuronal mechanisms of possible anxiety-relieving action of leptin are not known.Here, combining calcium imaging and opto- or chemogenetics in freely behaving mice, we investigated functions

…the relationship between the hormone leptin and H. perforatum, which inhibits the accumulation of fat tissue. Its effects on food intake and weight gain, as well as the mechanism underlying the interaction between leptin and NPY/AgRP genes in the hypothalamus, are poorly understood. There were five groups in the study.

Information processing is energetically expensive. In the mammalian brain, it is unclear how information coding and energy usage are regulated during food scarcity. I addressed this in the visual cortex of awake mice using whole-cell recordings and two-photon imaging to monitor layer 2/3 neuronal activity and ATP usage. I found that food restriction reduced synaptic ATP usage by 29% through a decrease in AMPA receptor conductance. Neuronal excitability was nonetheless preserved by a compensatory increase in input resistance and a depolarized resting membrane potential. Consequently, neurons sp

Sympathetic nerve activation of adrenergic receptors on fat is the major pathway the brain uses to drive non-shivering thermogenesis in brown adipose tissue and lipolysis in white fat. There is accumulating evidence that the peripheral nerve architecture inside of organs is plastic (can be remodeled) but the factors and conditions that regulate or result in remodeling are largely unknown. Particularly for fat, it remains unclear if nerves in fat can be remodeled in step with hyperplasia/trophy of adipose tissue as result of a prolonged energy surfeit. This talk will discuss our recent work ide

Puberty is a brain-driven phenomenon, which is under the control of sophisticated regulatory networks that integrate a large number of endogenous and environmental signals, including metabolic and nutritional cues. Puberty onset is tightly bound to the state of body energy reserves, and deregulation of energy/metabolic homeostasis is often associated with alterations in the timing of puberty. However, despite recent progress in the field, our knowledge of the specific molecular mechanisms and pathways whereby our brain decode metabolic information to modulate puberty onset remains fragmentary

…leptin) and how disease-associated mutations alter their function. Since human hypothalamic neurons can be produced in large numbers, are functionally responsive, have a human genome that can be readily edited, and are in culture environm