Topic: obesity

The regulation of body weight relies on homeostatic mechanisms that use a combination of internal signals and external cues to initiate and terminate food intake. Homeostasis depends on intricate communication between the body and the hypothalamus involving numerous neural and hormonal signals. However, there is growing evidence that higher-level cognitive function may also influence energy balance. For instance, research has shown that BMI is consistently linked to various brain, cognitive, and personality measures, implicating executive, reward, and attentional systems. Moreover, the rise in

Despite the profound effects of nutrition and physical activity on human health, our understanding of the molecules mediating the salutary effects of specific foods or activities remains remarkably limited. Here, we share our ongoing studies that use unbiased and high-resolution metabolomics technologies to uncover the molecules and molecular effectors of diet and exercise. We describe how exercise stimulates the production of Lac-Phe, a blood-borne signaling metabolite that suppresses feeding and obesity. Ablation of Lac-Phe biosynthesis in mice increases food intake and obesity after exercis

It is clear that the cause of obesity is a result of eating more than you burn. It is physics. What is more complex to answer is why some people eat more than others? Differences in our genetic make-up mean some of us are slightly more hungry all the time and so eat more than others. We now know that the genetics of body-weight, on which obesity sits on one end of the spectrum, is in actuality the genetics of appetite control. In contrast to the prevailing view, body-weight is not a choice. People who are obese are not bad or lazy; rather, they are fighting their biology.

The increasing prevalence of obesity and type 2 diabetes (T2D) and associated morbidity and mortality emphasizes the need for a more complete understanding of the mechanisms mediating energy homeostasis to accelerate the identification of new medications. Recent reports indicate that obesity medication, 5-hydroxytryptamine (5-HT, serotonin)2C receptor (5-HT2CR) agonist lorcaserin improves glycemic control in association with weight loss in obese patients with T2D. We examined whether lorcaserin has a direct effect on insulin sensitivity and how this effect is achieved. We clarify that lorcaser

Obesity and neurodegeneration lead to millions of premature deaths each year and lack broadly effective treatments. Obesity is largely caused by the abnormal function of cell populations in the hypothalamus that regulate appetite. We have developed methods generate human hypothalamic neurons from hPSCs to study how they respond to nutrients and hormones (e.g. 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

This open colloquia session is part of the special workshop entitled "Obesity at the Interface of Neuroscience and Physiology II". Abstract: Proopiomelanocortin (POMC)- and agouti related peptide (AgRP)-expressing neurons in the arcuate nucleus of the hypothalamus (ARH) are critical regulators of food intake and energy homeostasis. They rapidly integrate the energy state of the organism through sensing fuel availability via hormones, nutrient components and even rapidly upon sensory food perception. Importantly, they not only regulate feeding responses, but numerous autonomic responses includi

Reducing protein intake (and that of key amino acids) extends lifespan, especially during mid-life and early late-life. Yet, due to a powerful protein appetite, reducing protein in the diet leads to increased food intake, promoting obesity – which shortens lifespan. That is the protein paradox. In the talk I will bring together pieces of the jigsaw, including: specific nutrient appetites, protein leverage, macronutrient interactions on appetite and ageing, the role of branched-chain amino acids and FGF-21, and then I will conclude by showing how these pieces fit together and play out in the mo

Diets rich in sugar, salt, and fat alter taste perception and food intake, leading to obesity and metabolic disorders, but the molecular mechanisms through which this occurs are unknown. Here we show that in response to a high sugar diet, the epigenetic regulator Polycomb Repressive Complex 2.1 (PRC2.1) persistently reprograms the sensory neurons of D. melanogaster flies to reduce sweet sensation and promote obesity. In animals fed high sugar, the binding of PRC2.1 to the chromatin of the sweet gustatory neurons is redistributed to repress a developmental transcriptional network that modulates

Obesity, a multifaceted condition influenced by various environmental factors, represents a critical public health challenge. Among these factors, dietary choices and exposure to metabolic disrupting compounds (MDCs) play pivotal roles in shaping adipose tissue (AT) functions and its crosstalk with different organs, including the brain. The present collaborative research is integral to the HEAL ITALIA Project (Health Extended Alliance for Innovative Therapies, Advanced Lab-research, and Integrated Approaches of Precision Medicine). Our main objectives are twofold: i) to investigate the impact

Alzheimer’s disease (AD) is a complex disorder and multiple molecular mechanisms are involved in AD onset and progression. Recent evidences have suggested that metabolic alterations are an important pathological feature in AD. Likewise, diabetes and obesity, two metabolic illnesses, are risk factors for AD. These two diseases are associated with an expansion of visceral adipose tissue (VAT). Here, we hypothesize that the visceral adipose tissue may serve as a key communicator organ between the brain and peripheral metabolic disorders and affecting both types of disorders.We used histological s

The proportion of aged individuals in the general population is increasing, and non-communicable diseases like obesity are major contributors to mortality in older individuals. The WNIN/Ob obese rat exhibits a significantly reduced average lifespan of 15 months. Exploring molecular and biochemical characteristics of these rats can establish them as appropriate model for studying the neurobiology of aging and obesity.We investigated the growth characteristics and lifespan of WNIN/Obobese rats, examined neuronal-glial changes, levels of oxidative stress, antioxidant enzyme activity, and DNA dama

Metabolic Syndrome (MetS) and obesity correlate with cognitive impairment, heightening the susceptibility to cognitive decline and dementia. Noteworthy, cognitive impairment exacerbates weight management challenges in MetS, giving rise to a "cognitive decline-MetS" loop. Indeed, various cognitive and affective functions, including memory and executive functions, were found to be compromised in MetS, with underlying mechanistic pathways supporting a potential role of oxy-inflammatory signaling.Our research delves into the nuanced realm of cognitive alterations in MetS by examining the correlati