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Topic: Hunger

Seminar
6 seminars
Seminar · Neuroscience

The brain control of appetite: Can an old dog teach us new tricks?

Giles Yeo · MRC Metabolic Diseases Unit, University of Cambridge Metabolic Research Labs

Tue, Nov 2, 2021 · 15:00 UTC

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.

Seminar · Developmental Neuroscience

The development of hunger

Marcelo Dietrich · Yale

Mon, Oct 18, 2021 · 15:00 UTC

All mammals transition from breastfeeding to independent feeding during the lactation period. In humans and other mammals, this critical transition is important for later in life metabolic control and, consequently, for the development of many chronic conditions. Here, Dr. Dietrich will discuss the work of his lab studying the function of hypothalamic neurons involved in homeostatic control during the transition from breastfeeding to independent feeding. His work illuminates novel properties of hypothalamic neurons in early life, suggesting mechanisms by which early life events shape homeostat

Seminar · Brain Imaging

Estimation of current and future physiological states in insular cortex

Mark Andermann · Harvard University

Tue, Jun 29, 2021 · 16:00 UTC

Interoception, the sense of internal bodily signals, is essential for physiological homeostasis, cognition, and emotions. While human insular cortex (InsCtx) is implicated in interoception, the cellular and circuit mechanisms remain unclear. I will describe our recent work imaging mouse InsCtx neurons during two physiological deficiency states – hunger and thirst. InsCtx ongoing activity patterns reliably tracked the gradual return to homeostasis, but not changes in behavior. Accordingly, while artificial induction of hunger/thirst in sated mice via activation of specific hypothalamic neurons

Seminar · Neuroendocrinology

Central representations of protein availability regulating appetite and body weight control

Clemence Blouet · Wellcome-MRC Institute of Metabolic Science, University of Cambridge

Mon, Jun 14, 2021 · 15:00 UTC

Dietary protein quantity and quality greatly impact metabolic health via evolutionary-conserved mechanisms that ensure avoidance of amino acid imbalanced food sources, promote hyperphagia when dietary protein density is low, and conversely produce satiety when dietary protein density is high. Growing evidence support the emerging concept of protein homeostasis in mammals, where protein intake is maintained within a tight range independently of energy intake to reach a target protein intake. The behavioural and neuroendocrine mechanisms underlying these adaptations are unclear and form the focu

Seminar · Brain Imaging

Cortical estimation of current and future bodily states

Yoav Livneh · Weizmann Institute of Science

Mon, Nov 2, 2020 · 15:00 UTC

Interoception, the sense of internal bodily signals, is essential for physiological homeostasis, cognition, and emotions. Human neuroimaging studies suggest insular cortex plays a central role in interoception, yet the cellular and circuit mechanisms of its involvement remain unclear. We developed a microprism-based cellular imaging approach to monitor insular cortex activity in behaving mice across different physiological need states. We combine this imaging approach with manipulations of peripheral physiology, circuit-mapping, cell type-specific and circuit-specific manipulation approaches t

Seminar · Epigenetics

Epigenetic Reprogramming of Taste by Diet

Monica Dus · University of Michigan

Mon, Jul 20, 2020 · 15:00 UTC

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

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