̽��ֱ�� of Cambridge - diet

Map of brain’s appetite centre could enable new treatments for obesity and diabetes

Anonymous — Wed, 05 Feb 2025 16:00:15 +0000

Published today in Nature, this comprehensive resource, called HYPOMAP, provides an unparalleled view of the brain’s appetite centre and promises to accelerate the development of treatments for obesity and type 2 diabetes.

̽��ֱ��hypothalamus is often described as the brain’s ‘control centre’, orchestrating many of the body’s most vital processes. While much of our knowledge of the hypothalamus comes from animal studies, especially in mice, translating these findings to humans has long been a challenge. HYPOMAP bridges this gap by providing an atlas of the individual cells within the human hypothalamus. This resource not only charts over 450 unique cell types but also highlights key differences between the human and mouse hypothalamus — differences that have major implications for drug development.

“This is a game-changer for understanding the human hypothalamus,” said Professor Giles Yeo, senior author of the study from the Institute of Metabolic Science-Metabolic Research Laboratories (IMS-MRL) and MRC Metabolic Diseases Unit, ̽��ֱ�� of Cambridge.

“HYPOMAP confirms the critical role of the hypothalamus in body-weight regulation and has already allowed us to identify new genes linked to obesity. It gives us a roadmap to develop more effective, human-specific therapies.”

Together with researchers at the Max Planck Institute for Metabolism Research in Cologne, Professor Yeo and colleagues used cutting-edge technologies to analyse over 400,000 cells from 18 human donors. HYPOMAP allows researchers to pinpoint specific cell types, understand their genetic profiles, and explore how they interact with neighbouring cells. This detailed cellular resolution offers invaluable insights into the circuits that regulate appetite and energy balance, as well as other functions such as sleep and stress responses.

Comparison with a mouse hypothalamus atlas revealed both similarities and critical differences. Notably, some neurons in the mouse hypothalamus have receptors for GLP-1 — targets of popular weight-loss drugs like semaglutide — that are absent in humans.

"While drugs like semaglutide have shown success in treating obesity, newer therapies target multiple receptors such as GLP-1R and GIPR. Understanding how these receptors function specifically in the human hypothalamus is now crucial for designing safer and more effective treatments," said Dr Georgina Dowsett from the Max Planck Institute for Metabolism Research and formerly at the IMS-MRL.

“Our map of the human hypothalamus is an essential tool for basic and translational research,” added Professor Jens C. Brüning, Director at the Max Planck Institute. “It allows us to pinpoint which mouse nerve cells are most comparable to human cells, enabling more targeted preclinical studies.”

HYPOMAP’s open-access nature ensures that it will be an invaluable resource for scientists worldwide. By offering insights into the hypothalamus’s role in conditions ranging from obesity to cachexia (a wasting condition associated with several illness, which involves extreme loss of muscle and fat), it provides a foundation for tackling some of the most pressing health challenges of our time.

Dr John Tadross, Consultant Pathologist at Addenbrooke’s Hospital and lead author from IMS-MRL, said: “This is just the beginning. ̽��ֱ��atlas itself is a milestone, but what could really make a difference for patients is understanding how the hypothalamus changes in people who are overweight or underweight. This could fundamentally shift our approach to metabolic health and enable more personalised therapies.”

With HYPOMAP, researchers have a new tool to unlock the secrets of the human brain’s metabolic control centre. By better understanding the human hypothalamus, science takes a significant step toward combating obesity, type 2 diabetes, and related conditions.

Reference
Tadross, JA, Steuernagel, L & Dowsett, GKC et al. A comprehensive spatio-cellular map of the human hypothalamus. Nature; 5 Feb 2025; DOI: 10.1038/s41586-024-08504-8

Adapted from a story by the Institute of Metabolic Science-Metabolic Research Laboratories and the Max Planck Institute for Metabolism Research

Scientists have created the most detailed map to date of the human hypothalamus, a crucial brain region that regulates body weight, appetite, sleep, and stress.

HYPOMAP confirms the critical role of the hypothalamus in body-weight regulation and has already allowed us to identify new genes linked to obesity

Giles Yeo

Sander Dalhuisen

Person holding burger bun with vegetables and meat

̽��ֱ��text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

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Boost your life in 2025: Top tips for a healthier body and mind from Cambridge experts

jg533 — Thu, 02 Jan 2025 09:16:07 +0000

Five Cambridge experts share their top tips on ways to boost your body and mind, backed up by their own research

Ultra-processed food makes up almost two-thirds of calorie intake of UK adolescents

cjb250 — Wed, 17 Jul 2024 01:30:13 +0000

̽��ֱ��study found that UPF consumption was highest among adolescents from deprived backgrounds, those of white ethnicity, and younger adolescents.

UPFs are food items that are manufactured from industrial substances and contain additives such as preservatives, sweeteners, colourings, flavourings, and emulsifiers. UPFs vary greatly, but tend to indicate poor dietary quality, with higher levels of added sugars, saturated fat, and sodium, as well as decreased fibre, protein, and micronutrient content. They have been suggested as one of the key drivers of the global rise in diseases such as obesity, type 2 diabetes, and cancer.

Globally, the availability and sales of UPFs have increased over time and previous evidence suggests that this has led to increased consumption among adolescents. To look at trends within the UK, researchers from Cambridge and Bristol analysed data from four-day food diaries of almost 3,000 adolescents in the UK National Diet and Nutrition Survey between 2008/09 and 2018/19.

In research published today in the European Journal of Nutrition, the researchers found that a mean of 66% of adolescents’ energy intake came from UPF consumption during this period, though there was a slight fall from 68% to 63% between 2008/09 and 2018/2019.

Parents’ occupation, ethnic group and UK region all influenced the proportion of calorie intake from UPFs:

Adolescents from disadvantaged backgrounds consumed a higher proportion of their calorie intake from UPFs compared to adolescents from less disadvantaged backgrounds (68.4% compared with 63.8%).
Adolescents from a non-white ethnicity consumed a lower proportion of their calorie intake from UPFs (59.0% compared with 67.3%).
Adolescents living in the North of England consumed a higher proportion of their calorie intake from UPFs compared with those living in the South of England and London (67.4% compared with 64.1%).
18-year-olds consumed a lower proportion of their calorie intake from UPFs compared with 11-year-olds (63.4% compared with 65.6%).

Dr Yanaina Chavez-Ugalde from the Medical Research Council (MRC) Epidemiology Unit at the ̽��ֱ�� of Cambridge, the study’s first author, said: “Adolescents’ food patterns and practices are influenced by many factors, including their home environment, the marketing they are exposed to and the influence of their friends and peers. But adolescence is also an important time in our lives where behaviours begin to become ingrained.

“It’s clear from our findings that ultra-processed foods make up the majority of adolescents’ diets, and their consumption is at a much higher level than is ideal, given their potential negative health impacts.”

̽��ֱ��researchers argue that the observed reduction in UPF intake pre-pandemic could be partly explained by an increased public awareness and health concerns associated with sugar consumption, government-led campaigns, sugar-taxes in other countries and the reformulation of sugary drinks to reduce their sugar content.

Dr Esther van Sluijs from the MRC Epidemiology Unit at Cambridge, joint senior author, said: “Ultra-processed foods offer convenient and often cheaper solutions to time- and income-poor families, but unfortunately many of these foods also offer poor nutritional value. This could be contributing to the inequalities in health we see emerging across childhood and adolescence.”

Dr Zoi Toumpakari from the Centre for Exercise, Nutrition and Health Sciences at the ̽��ֱ�� of Bristol, joint senior author, added: “Our findings suggest that disparities in consumption of ultra-processed foods are not just down to individual choices. We hope this evidence can help guide policymakers in designing more effective policies to combat the negative effects of ultra-processed food consumption among youth and the ripple effects this has on public health.”

This study was largely funded by the National Institute for Health and Care Research School for Public Health Research.

Reference
Chavez-Ugalde, Y et al. Ultra-processed food consumption in UK adolescents: distribution, trends, and sociodemographic correlates using the National Diet and Nutrition Survey 2008/09 to 2018/19. Eur J Nutr; 17 Jul 2024; DOI: 10.1007/s00394-024-03458-z

Adolescents consume around two-thirds of their daily calories from ultra-processed foods (UPFs), new research from the Universities of Cambridge and Bristol has found.

Ultra-processed foods make up the majority of adolescents’ diets, and their consumption is at a much higher level than is ideal, given their potential negative health impacts

Yanaina Chavez-Ugalde

Juanmonino (Getty Images)

Boy eating a burger

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Exercising during pregnancy normalises eating behaviours in offspring from obese mice

Anonymous — Tue, 04 Jun 2024 18:00:43 +0000

Previous studies in both humans and animal models have shown that the offspring of mothers living with obesity have a higher risk of developing obesity and type 2 diabetes themselves when they grow up. While this relationship is likely to be the result of a complex relationship between genetics and environment, emerging evidence has implicated that maternal obesity in pregnancy can disrupt the baby’s hypothalamus—the region of the brain responsible for controlling food intake and energy regulation.

In animal models, offspring exposed to overnutrition during key periods of development eat more when they grow up, but little is known about the molecular mechanisms that lead to these changes in eating behaviour.

In a study published today in PLOS Biology, researchers from the Institute of Metabolic Science and the MRC Metabolic Diseases Unit at the ̽��ֱ�� of Cambridge found that mice born from obese mothers had higher levels of the microRNA miR-505-5p in their hypothalamus—from as early as the fetal stage into adulthood. ̽��ֱ��offspring of obese mothers chose to eat more specifically of foods that were high in fat, which is consistent with fat sensing being disrupted in the hypothalamus.

Dr Laura Dearden from the Institute of Metabolic Science, the study’s first author, said: “Our results show that obesity during pregnancy causes changes to the baby's brain that makes them eat more high fat food in adulthood and more likely to develop obesity.”

Senior author Professor Susan Ozanne from the MRC Metabolic Diseases Unit and Institute of Metabolic Science said: “Importantly, we showed that moderate exercise, without weight loss, during pregnancies complicated by obesity prevented the changes to the baby's brain.”

Cell culture experiments showed that miR-505-5p levels can be influenced by exposing hypothalamic neurons to long-chain fatty acids and insulin, which are both high in pregnancies complicated by obesity. ̽��ֱ��researchers identified miR-505-5p as a regulator of pathways involved in fatty acid uptake and metabolism – high levels of the miRNA make the offspring brain unable to sense when they are eating high fat foods. Several of the genes that miR-505-5p regulates are associated with high body mass index in human genetic studies, showing these same changes in humans can cause obesity.

̽��ֱ��study is one of the first to demonstrate the molecular mechanisms linking nutritional exposure in utero to eating behaviour.

Dr Dearden added: “While our work was only carried out in mice, it may help us understand why the children of mothers living with obesity are more likely to become obese themselves, with early life exposures, genetics and current environment all being contributing factors.”

Reference
Dearden, L et al. Maternal obesity increases hypothalamic miR-505-5p expression in mouse offspring leading to altered fatty acid sensing and increased intake of high-fat food. PLOS Biology; 4 Jun 2024; DOI: 10.1371/journal.pbio.3002641

Adapted from a press release by PLOS Biology

Maternal obesity in pregnancy changes the eating behaviours of offspring by increasing long-term levels of particular molecules known as microRNAs in the part of the brain that controls appetite – but this can be changed by exercise during pregnancy, a study in obese mice has suggested.

We showed that moderate exercise, without weight loss, during pregnancies complicated by obesity prevented the changes to the baby's brain

Susan Ozanne

Engin_Akyurt (Pixabay)

Fast food meal of burger and fries

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AI predicts healthiness of food menus

cjb250 — Fri, 08 Mar 2024 08:00:27 +0000

Cambridge researchers have used artificial intelligence to predict the healthiness of café, takeaway and restaurant menus at outlets across Britain and used this information to map which of its local authorities have the most and least healthy food environments.

Scientists identify how fasting may protect against inflammation

cjb250 — Tue, 30 Jan 2024 09:55:30 +0000

In research published in Cell Reports, the team describes how fasting raises levels of a chemical in the blood known as arachidonic acid, which inhibits inflammation. ̽��ֱ��researchers say it may also help explain some of the beneficial effects of drugs such as aspirin.

Scientists have known for some time that our diet – particular a high-calorie Western diet – can increase our risk of diseases including obesity, type 2 diabetes and heart disease, which are linked to chronic inflammation in the body.

Inflammation is our body’s natural response to injury or infection, but this process can be triggered by other mechanisms, including by the so-called ‘inflammasome’, which acts like an alarm within our body’s cells, triggering inflammation to help protect our body when it senses damage. But the inflammasome can trigger inflammation in unintentional ways – one of its functions is to destroy unwanted cells, which can result in the release of the cell’s contents into the body, where they trigger inflammation.

Professor Clare Bryant from the Department of Medicine at the ̽��ֱ�� of Cambridge said: “We’re very interested in trying to understand the causes of chronic inflammation in the context of many human diseases, and in particular the role of the inflammasome.

“What's become apparent over recent years is that one inflammasome in particular – the NLRP3 inflammasome – is very important in a number of major diseases such as obesity and atherosclerosis, but also in diseases like Alzheimer's and Parkinson's disease, many of the diseases of older age people, particularly in the Western world.”

Fasting can help reduce inflammation, but the reason why has not been clear. To help answer this question, a team led by Professor Bryant and colleagues at the ̽��ֱ�� of Cambridge and National Institute for Health in the USA studied blood samples from a group of 21 volunteers, who ate a 500kcal meal then fasted for 24 hours before consuming a second 500kcal meal.

̽��ֱ��team found that restricting calorie intake increased levels of a lipid known as arachidonic acid. Lipids are molecules that play important roles in our bodies, such as storing energy and transmitting information between cells. As soon as individuals ate a meal again, levels of arachidonic acid dropped.

When the researchers studied arachidonic acid’s effect in immune cells cultured in the lab, they found that it turns down the activity of the NLRP3 inflammasome. This surprised the team as arachidonic acid was previously thought to be linked with increased levels of inflammation, not decreased.

Professor Bryant, a Fellow of Queens’ College, Cambridge, added: “This provides a potential explanation for how changing our diet – in particular by fasting – protects us from inflammation, especially the damaging form that underpins many diseases related to a Western high calorie diet.

“It’s too early to say whether fasting protects against diseases like Alzheimer's and Parkinson's disease as the effects of arachidonic acid are only short-lived, but our work adds to a growing amount of scientific literature that points to the health benefits of calorie restriction. It suggests that regular fasting over a long period could help reduce the chronic inflammation we associate with these conditions. It's certainly an attractive idea.”

̽��ֱ��findings also hint at one mechanism whereby a high calorie diet might increase the risk of these diseases. Studies have shown that some patients that have a high fat diet have increased levels of inflammasome activity.

“There could be a yin and yang effect going on here, whereby too much of the wrong thing is increasing your inflammasome activity and too little is decreasing it,” said Professor Bryant. “Arachidonic acid could be one way in which this is happening.”

̽��ֱ��researchers say the discovery may also offer clues to an unexpected way in which so-called non-steroidal anti-inflammatory drugs such as aspirin work. Normally, arachidonic acid is rapidly broken down in the body, but aspirin stops this process, which can lead to an increase in levels of arachidonic acid, which in turn reduce inflammasome activity and hence inflammation.

Professor Bryant said: “It’s important to stress that aspirin should not be taken to reduce risk of long terms diseases without medical guidance as it can have side-effects such as stomach bleeds if taken over a long period.”

̽��ֱ��research was funded by Wellcome, the Medical Research Council and the US National Heart, Lung, and Blood Institute Division of Intramural Research.

Reference
Pereira, M & Liang, J et al. Arachidonic acid inhibition of the NLRP3 inflammasome is a mechanism to explain the anti-inflammatory effects of fasting. Cell Reports; 23 Jan 2024; DOI: 10.1016/j.celrep.2024.113700

Cambridge scientists may have discovered a new way in which fasting helps reduce inflammation – a potentially damaging side-effect of the body’s immune system that underlies a number of chronic diseases.

Our work adds to a growing amount of scientific literature that points to the health benefits of calorie restriction

Clare Bryant

Carol Yepes (Getty Images)

Intermittent fasting conceptual image

Yes

Ancient DNA reveals reason for high MS and Alzheimer's rates in Europe

jg533 — Wed, 10 Jan 2024 16:06:31 +0000

Researchers have created the world’s largest ancient human gene bank, and used it to map the historical spread of genes – and diseases – over time as populations migrated.

No evidence that physical activity calorie-equivalent labelling changes food purchasing – study

cjb250 — Wed, 09 Nov 2022 08:30:30 +0000

More than three in five UK adults are overweight or obese, increasing their risk of diseases such as type 2 diabetes and cancer. A major factor that contributes to this is excess energy intake – in other words, eating too many calories. Measures that can help reduce energy intake could help tackle the obesity problem.

In the UK, adults eat as many as a third of their meals out of home, including in workplace cafeterias, and these meals are often much higher in calories than meals eaten at home. Since April 2022 calorie labelling is now required on food and drink served out of the home in businesses employing 250 or more people. While many people welcome this information, evidence for its effectiveness in reducing calories purchased or consumed is limited in quantity and quality. For example, two previous studies conducted by the authors in nine worksite cafeterias found no evidence for an effect of simple calorie labelling (kcal) on calories purchased.

Another option is to show the amount of exercise required to burn off these calories – so-called PACE (physical activity calorie-equivalent) labels – for example, a 1014kcal ‘large battered haddock’ portion would take upwards of five hours walking (278 minutes) to burn off. A recent systematic review – a type of study that brings together existing evidence – concluded that PACE labels may reduce energy selected from menus and decrease the energy consumed when compared with simple calorie labels or no labels, but only one of the 15 studies reviewed was in a ‘real world’ setting.

To explore whether PACE levels can make a difference in real world settings, researchers from the ̽��ֱ�� of Cambridge’s Behaviour and Health Research Unit carried out an experiment across 10 workplace cafeterias in England over a 12 week period in 2021. Their results are published today in PLOS Medicine.

̽��ֱ��team collected baseline sales data for a period of business-as-usual for the cafeterias ahead of the experiment. During this period, most labels and menus featured only the product name and price, though some products included standardised front-of-pack nutrition labels on branded and in-house products. During the intervention period the ten cafeterias included calorie information and PACE labels alongside food and drinks items and on items including hot meals, sandwiches, cold drinks and desserts. These labels displayed the minutes of walking that would be needed to burn off the calories in the product.

̽��ֱ��team found no evidence that including PACE labels resulted in an overall change in energy purchased from labelled items. However, there was a great deal of variability, with one cafeteria reporting a fall per transaction of 161kcal and another an increase of 69kcal, while five of the cafeterias reported no significant change.

First author Dr James Reynolds from the School of Psychology, Aston ̽��ֱ��, who carried out the research while at Cambridge, said: “Although we found that showing the amount of exercise required to burn off calories made little difference to the number of calories purchased – and, we can assume, eaten and drunk – there was considerable variability between cafeterias. This suggests that other factors may have influenced the effectiveness of these labels, such as the type of food sold in the cafeteria or the characteristics of those using them.”

̽��ֱ��number of calories purchased from items that did not feature the PACE labels did not change and the labels made little difference to the revenue for the cafeterias – just a small increase of 3p per transaction.

Senior author Professor Dame Theresa Marteau, Director of the Behaviour and Health Research Unit and Bye-Fellow of Christ’s College, ̽��ֱ�� of Cambridge, said: “This is the largest study in a real world setting to look at the impact of PACE labels on food and drink purchases, examining 250,000 transactions across 10 worksite cafeterias. ̽��ֱ��findings suggest that PACE labels, contrary to expectations, may have little or no impact on the food people buy in worksite cafeterias.”

Reference
Reynolds, JP et al. Evaluation of physical activity calorie equivalent (PACE) labels’ impact on energy purchased in cafeterias: a stepped-wedge randomised controlled trial. PLOS Med; 8 Nov 2022; DOI: 10.1371/journal.pmed.1004116

An experiment carried out across ten workplace cafeterias found no significant change in the overall number of calories purchased when food and drink labels showed the amount of physical activity required to burn off their calories.

̽��ֱ��findings suggest that physical activity calorie-equivalent labels, contrary to expectations, may have little or no impact on the food people buy in worksite cafeterias

Theresa Marteau

̽��ֱ�� of Cambridge

PACE labels alongside menus

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – as here, on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

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