John Speakman
I run 2 research groups. One at the Chinese Academy of Sciences Institute of Genetics and Developmental Biology in Beijing where I am a '1000 talents' A-grade Professor, and a second group at the University of Aberdeen in Scotland, UK. My main research interest is in energy balance: the factors that determine energy expenditure and food intake, and hence variation in fat storage. We have a particular interest in the factors that limit food intake and the implications of energy demands for life histories and ageing. Our work stretches from the gene to the individual organism and includes studies of wild and captive animals as well as humans. We have an ongoing research program to study te impacts of caloric restriction. The lab in Aberdeen (www.abdn.ac.uk/energetics-research) includes a facility for measurement of stable isotopes in the context of applications of the doubly-labelled water method to measure free-living energy demands. We collaborate with groups worldwide to apply this methodology.
Address: Beijing, Beijing, China
Address: Beijing, Beijing, China
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Papers by John Speakman
adiposity.Wedesigned10 diets varying from1%to 20%protein combinedwith either 60%or 20%fat, contrasting
the expectation that very lowprotein did not cause increased foodintake. Althoughthese mice had activated
hunger signaling, they ate less food, resulting in decreasedbodyweight and improved glucose tolerance but not
increased frailty, even under 60%fat.Moreover, they did not showhyperphagia when returned to a 20%protein
diet, which could be mimicked by treatment with rapamycin. Intracerebroventricular injection of AAV-S6K1
significantly blunted the decrease in both food intake and body weight in mice fed 1% protein, an effect not
observed with inhibition of eIF2a, TRPML1, and Fgf21 signaling. Hence, the1%protein diet induced decreased
food intake and body weight via a mechanism partially dependent on hypothalamic mTOR signaling.
adiposity.Wedesigned10 diets varying from1%to 20%protein combinedwith either 60%or 20%fat, contrasting
the expectation that very lowprotein did not cause increased foodintake. Althoughthese mice had activated
hunger signaling, they ate less food, resulting in decreasedbodyweight and improved glucose tolerance but not
increased frailty, even under 60%fat.Moreover, they did not showhyperphagia when returned to a 20%protein
diet, which could be mimicked by treatment with rapamycin. Intracerebroventricular injection of AAV-S6K1
significantly blunted the decrease in both food intake and body weight in mice fed 1% protein, an effect not
observed with inhibition of eIF2a, TRPML1, and Fgf21 signaling. Hence, the1%protein diet induced decreased
food intake and body weight via a mechanism partially dependent on hypothalamic mTOR signaling.
adiposity.Wedesigned10 diets varying from1%to 20%protein combinedwith either 60%or 20%fat, contrasting
the expectation that very lowprotein did not cause increased foodintake. Althoughthese mice had activated
hunger signaling, they ate less food, resulting in decreasedbodyweight and improved glucose tolerance but not
increased frailty, even under 60%fat.Moreover, they did not showhyperphagia when returned to a 20%protein
diet, which could be mimicked by treatment with rapamycin. Intracerebroventricular injection of AAV-S6K1
significantly blunted the decrease in both food intake and body weight in mice fed 1% protein, an effect not
observed with inhibition of eIF2a, TRPML1, and Fgf21 signaling. Hence, the1%protein diet induced decreased
food intake and body weight via a mechanism partially dependent on hypothalamic mTOR signaling.
weight regulation remain unresolved, with different
studies suggesting increased dietary fat, increased
carbohydrates (particularly sugars), or reduced protein
may all stimulate overconsumption and drive
obesity. Weexposed C57BL/6 mice to 29 different diets
varying from 8.3% to 80% fat, 10% to 80% carbohydrate,
5% to 30% protein, and 5% to 30% sucrose.
Only increased dietary fat content was associated
with elevated energy intake and adiposity. This
response was associated with increased gene
expression in the 5-HT receptors, and the dopamine
and opioid signaling pathways in the hypothalamus.
We replicated the core findings in four other mouse
strains (DBA/2, BALB/c, FVB, and C3H). Mice regulate
their food consumption primarily to meet an energy
rather than a protein target, but this system can
be over-ridden by hedonic factors linked to fat, but
not sucrose, consumption.
adiposity.Wedesigned10 diets varying from1%to 20%protein combinedwith either 60%or 20%fat, contrasting
the expectation that very lowprotein did not cause increased foodintake. Althoughthese mice had activated
hunger signaling, they ate less food, resulting in decreasedbodyweight and improved glucose tolerance but not
increased frailty, even under 60%fat.Moreover, they did not showhyperphagia when returned to a 20%protein
diet, which could be mimicked by treatment with rapamycin. Intracerebroventricular injection of AAV-S6K1
significantly blunted the decrease in both food intake and body weight in mice fed 1% protein, an effect not
observed with inhibition of eIF2a, TRPML1, and Fgf21 signaling. Hence, the1%protein diet induced decreased
food intake and body weight via a mechanism partially dependent on hypothalamic mTOR signaling.
adiposity.Wedesigned10 diets varying from1%to 20%protein combinedwith either 60%or 20%fat, contrasting
the expectation that very lowprotein did not cause increased foodintake. Althoughthese mice had activated
hunger signaling, they ate less food, resulting in decreasedbodyweight and improved glucose tolerance but not
increased frailty, even under 60%fat.Moreover, they did not showhyperphagia when returned to a 20%protein
diet, which could be mimicked by treatment with rapamycin. Intracerebroventricular injection of AAV-S6K1
significantly blunted the decrease in both food intake and body weight in mice fed 1% protein, an effect not
observed with inhibition of eIF2a, TRPML1, and Fgf21 signaling. Hence, the1%protein diet induced decreased
food intake and body weight via a mechanism partially dependent on hypothalamic mTOR signaling.
adiposity.Wedesigned10 diets varying from1%to 20%protein combinedwith either 60%or 20%fat, contrasting
the expectation that very lowprotein did not cause increased foodintake. Althoughthese mice had activated
hunger signaling, they ate less food, resulting in decreasedbodyweight and improved glucose tolerance but not
increased frailty, even under 60%fat.Moreover, they did not showhyperphagia when returned to a 20%protein
diet, which could be mimicked by treatment with rapamycin. Intracerebroventricular injection of AAV-S6K1
significantly blunted the decrease in both food intake and body weight in mice fed 1% protein, an effect not
observed with inhibition of eIF2a, TRPML1, and Fgf21 signaling. Hence, the1%protein diet induced decreased
food intake and body weight via a mechanism partially dependent on hypothalamic mTOR signaling.
weight regulation remain unresolved, with different
studies suggesting increased dietary fat, increased
carbohydrates (particularly sugars), or reduced protein
may all stimulate overconsumption and drive
obesity. Weexposed C57BL/6 mice to 29 different diets
varying from 8.3% to 80% fat, 10% to 80% carbohydrate,
5% to 30% protein, and 5% to 30% sucrose.
Only increased dietary fat content was associated
with elevated energy intake and adiposity. This
response was associated with increased gene
expression in the 5-HT receptors, and the dopamine
and opioid signaling pathways in the hypothalamus.
We replicated the core findings in four other mouse
strains (DBA/2, BALB/c, FVB, and C3H). Mice regulate
their food consumption primarily to meet an energy
rather than a protein target, but this system can
be over-ridden by hedonic factors linked to fat, but
not sucrose, consumption.