Sable Systems

And as always, my lecture covered metabolic allometry and the correct analysis of metabolic data for animals with different body masses. Of course, unlike the legacy companies, we will never divide metabolic data by body mass, disproven since 1849! 2/2

In our latest metabolic phenotyping course, taught as always by true experts in the field, Dr. Marshall McCue (our very stable isotope expert) enthralls the eager course attendees with his discussion of the thermal neutral zone 😎 1/2

Strange times indeed 

Follow the crumbs

This is so, so sad. And so unnecessary. What a tragedy  for common sense, reason and simple decency. If I were lucky enough to be Canadian I would probably feel the same way. 

Another useful reminder to not divide metabolic rate by body mass!

This classic work by Regnault & Reiset was published in 1849. It conclusively showed that correcting metabolic rate for body mass by dividing by body mass is a worthless & misleading technique. They knew better, unlike the legacy metabolic phenotyping companies today!

High-fat diet increases circulating palmitic acid produced by gut Bacteroides thetaiotaomicron to promote thrombosis Huang et al. demonstrate that elevated circulating palmitic acid (PA) induces hypercoagulability by inhibiting activated protein C (APC) and enhancing platelet activation. High-fat diet increases gut ...

More intriguing Promethion-powered research from Dr. R Lai & colleagues at the Chinese Academy of Sciences - gut Bacteroides thetaiotaomicron can raise circulating palmitate & promote thrombosis under high-fat diet! 🧪 www.cell.com/cell-reports...

Lack of glutamate neurotransmission in melanin-concentrating hormone neurons alters mouse reproduction and metabolism in a sex-specific manner - Biology of Sex Differences Melanin-concentrating hormone (MCH) is a neuropeptide important for the regulation of metabolism, sleep, circadian rhythms, and other body functions. MCH neurons contain the excitatory neurotransmitter glutamate, which is released via vesicular glutamate transporter 2 (VGLUT2). The release of glutamate from MCH neurons is known to play a role in metabolism in males, but its action in female physiology has not been determined. Furthermore, little is known about the role of glutamate release from MCH neurons in reproductive function. We developed a new transgenic mouse model that expresses Cre recombinase driven by the MCH gene (Pmch) and deleted Vglut2 from the MCH neurons. We then assessed reproductive and metabolic function in both sexes. Females exhibited late-onset leanness, delayed sexual maturation, and increased latency to pregnancy. On a high-fat diet, males showed improved insulin resistance, and both sexes displayed an improved daily pattern of food intake. These findings highlight the importance of considering sex as a relevant biological variable in MCH neuronal function. Melanin-concentrating hormone (MCH) neurons contribute to the regulation of a diverse array of physiological functions including glucose and energy homeostasis. MCH neurons express genes involved in the synthesis, packaging, and release of glutamate, the brain’s predominant excitatory neurotransmitter. Deletion of vesicular glutamate transporter 2 (VGLUT2, Slc17a6 gene) in MCH neurons of male mice results in a hypophagic, hyperactive, lean phenotype. However, the metabolic and reproductive effects of VGLUT2 deletion in females have not been fully addressed. Previous studies have utilized Pmch-Cre mice generated using a bacterial artificial chromosome (BAC). The loci of insertion for the BAC are random and may fail to recapitulate epigenetic regulation at the native gene locus. Here, we generated a novel knock-in Pmch-iCre mouse model and investigated the effects of deleting Slc17a6 from MCH neurons in both male and female mice. Assessment of sexual maturation, fertility, glucose homeostasis and energy balance (food intake, body composition, energy expenditure, locomotion, glucose and fat oxidation) on regular chow and high fat diet (HFD) were performed in both sexes. Lack of glutamate neurotransmission in MCH neurons (PmchΔVglut2 mice) delays puberty onset and completion in female, but not male mice. PmchΔVglut2 females were also protected against (HFD)-induced disruption of estrous cycles. On a regular chow diet, neither male nor female PmchΔVglut2 mice showed differences in body weight, food intake, or lean and fat masses compared to littermate controls until 20 weeks of age. At 24 weeks of age, PmchΔVglut2 females exhibited reduced total body mass, and males had lower fat mass. PmchΔVglut2 female mice also gained less weight on HFD than littermate controls. An attenuation of HFD-induced disruption of daily feeding pattern was observed in PmchΔVglut2 mice of both sexes, while only males were protected against insulin resistance on HFD. Glutamate neurotransmission from MCH neurons has a sex-specific role in sexual maturation, fertility, typical weight gain trajectory, and HFD-induced weight gain and insulin resistance. In addition, a sex-independent role in daily feeding pattern was observed.

More interesting Promethion-powered research from Dr. Elias & colleagues at University of Michigan - glutamate release from MCH neurons drives sex-specific effects on reproduction & metabolism! 🧪 bsd.biomedcentral.com/articles/10....

More intriguing Promethion-powered science from O. MacDougald & colleagues at University of Michigan - FGF21, soluble TGFBR2 & ambient temperature shape metabolic dysfunction in lipodystrophic mice! 🧪 insight.jci.org/articles/vie...

She has a way with words.

One of my favorite anecdotes from THE PREHISTORY OF THE FAR SIDE: "That doesn't sound like the Jane Goodall we know."

Acute exogenous acyl-GIP treatment enhances lipid handling and fatty acid oxidation by involving brown fat | EMBO reports imageimageAcute exogenous acyl-GIP administration promotes brown adipose tissue (BAT) lipid uptake during lipid tolerance tests, augmenting whole-body lipid handling and increases whole-body fatty acid oxidation during routine metabolism in male ...

Cool new research from the lab of Dr. Jacqueline Beaudry, PhD led by Sulayman Lyons looks at brown fat. I may not always fully understand this very foundational science, but I do understand the importance of doing this work. 🧪#ResearchMatters www.embopress.org/doi/full/10....

Lack of glutamate neurotransmission in melanin-concentrating hormone neurons alters mouse reproduction and metabolism in a sex-specific manner - Biology of Sex Differences Melanin-concentrating hormone (MCH) is a neuropeptide important for the regulation of metabolism, sleep, circadian rhythms, and other body functions. MCH neurons contain the excitatory neurotransmitter glutamate, which is released via vesicular glutamate transporter 2 (VGLUT2). The release of glutamate from MCH neurons is known to play a role in metabolism in males, but its action in female physiology has not been determined. Furthermore, little is known about the role of glutamate release from MCH neurons in reproductive function. We developed a new transgenic mouse model that expresses Cre recombinase driven by the MCH gene (Pmch) and deleted Vglut2 from the MCH neurons. We then assessed reproductive and metabolic function in both sexes. Females exhibited late-onset leanness, delayed sexual maturation, and increased latency to pregnancy. On a high-fat diet, males showed improved insulin resistance, and both sexes displayed an improved daily pattern of food intake. These findings highlight the importance of considering sex as a relevant biological variable in MCH neuronal function. Melanin-concentrating hormone (MCH) neurons contribute to the regulation of a diverse array of physiological functions including glucose and energy homeostasis. MCH neurons express genes involved in the synthesis, packaging, and release of glutamate, the brain’s predominant excitatory neurotransmitter. Deletion of vesicular glutamate transporter 2 (VGLUT2, Slc17a6 gene) in MCH neurons of male mice results in a hypophagic, hyperactive, lean phenotype. However, the metabolic and reproductive effects of VGLUT2 deletion in females have not been fully addressed. Previous studies have utilized Pmch-Cre mice generated using a bacterial artificial chromosome (BAC). The loci of insertion for the BAC are random and may fail to recapitulate epigenetic regulation at the native gene locus. Here, we generated a novel knock-in Pmch-iCre mouse model and investigated the effects of deleting Slc17a6 from MCH neurons in both male and female mice. Assessment of sexual maturation, fertility, glucose homeostasis and energy balance (food intake, body composition, energy expenditure, locomotion, glucose and fat oxidation) on regular chow and high fat diet (HFD) were performed in both sexes. Lack of glutamate neurotransmission in MCH neurons (PmchΔVglut2 mice) delays puberty onset and completion in female, but not male mice. PmchΔVglut2 females were also protected against (HFD)-induced disruption of estrous cycles. On a regular chow diet, neither male nor female PmchΔVglut2 mice showed differences in body weight, food intake, or lean and fat masses compared to littermate controls until 20 weeks of age. At 24 weeks of age, PmchΔVglut2 females exhibited reduced total body mass, and males had lower fat mass. PmchΔVglut2 female mice also gained less weight on HFD than littermate controls. An attenuation of HFD-induced disruption of daily feeding pattern was observed in PmchΔVglut2 mice of both sexes, while only males were protected against insulin resistance on HFD. Glutamate neurotransmission from MCH neurons has a sex-specific role in sexual maturation, fertility, typical weight gain trajectory, and HFD-induced weight gain and insulin resistance. In addition, a sex-independent role in daily feeding pattern was observed.

More interesting Promethion-powered research from C. Elias & colleagues at University of Michigan - glutamate release from MCH neurons drives sex-specific effects on reproduction & metabolism! 🧪 bsd.biomedcentral.com/articles/10....

More intriguing Promethion-powered science from O. MacDougald & colleagues at University of Michigan - FGF21, soluble TGFBR2 & ambient temperature shape metabolic dysfunction in lipodystrophic mice! 🧪 insight.jci.org/articles/vie...

A UFD1 variant encoding a microprotein modulates UFD1f and IPMK ubiquitination to play pivotal roles in anti-stress responses - Nature Communications Some small mRNA isoforms regulate cellular responses to stress. Here, Li et al. identify UFD1s, a stress responsive micro-RNA that encodes a conserved microprotein that regulates ubiquitination of full length UFD1, promotes autophagy and fatty acid oxidation, and acts to alleviate NASH progression in mice.

More intriguing Promethion-powered research from Dr. L Chen & colleagues at the University of Science and Technology (China) - a stress-responsive UFD1 microprotein tunes ubiquitination, promotes autophagy & eases NASH in mice. 🧪 www.nature.com/articles/s41...

More fascinating Promethion-powered research from Dr. A Zorzano & colleagues at the Institute for Research in Biomedicine (Barcelona) - Neuritin 1 from brown fat acts locally to boost thermogenesis & lower fat mass in mice! 🧪 www.nature.com/articles/s41...

A consensus guide to preclinical indirect calorimetry experiments Nature Metabolism - The authors highlight inconsistencies and divergencies in the literature reporting data on indirect calorimetry for studies on whole-body energy homeostasis, and propose...

..., "quantifying" activity by beam-breaks (meaningless given the diversity of inter-beam distances), &... I could go on & on. This is a landmark paper & long overdue. Congratulations to all involved! Link: www.nature.com/articles/s42...

I can't applaud this enough! Announcing the end of a decades-long era of legacy system vendors treating metabolic rate as isometric with respect to body mass (it's allometric & "normalizing" it by dividing by body mass is crazily misleading & awe-inspiringly ignorant)...

#metabolism #obesityresearch #openscience #datastandards #biomedicalresearch #reproducibility #energyexpenditure #indirectcalorimetry #fairdata #consensusscience | Alex Banks Online today in Nature Metabolism: 🚨 New Global Standards for Metabolic Research: Unifying Indirect Calorimetry Experiments! 🔬🧬 Understanding how our bodies use energy is vital for tackling obesity, ...

Announcing a landmark paper from Alex Banks & colleagues on standardizing preclinical metabolic phenotyping data! 🧪 www.linkedin.com/posts/alex-b...

Really excited to announce that I've accepted an Assistant Professor position in the Department of Nutritional Sciences in the Faculty of Medicine at the University of Toronto! Looking forward to venturing north (🥶) & building out my own research group focused on human nutrition & metabolism 🥳

The source of dietary fat influences anti-tumour immunity in obese mice - Nature Metabolism This study shows that animal-based high-fat diets accelerate tumour growth and impair anti-tumour response to melanoma in obese mice, whereas plant-based high-fat diets do not.

Nature MS#2 today - More interesting Promethion-powered science from Dr. L Lynch & colleagues - butter-based HFD suppresses NK/CD8 anti-tumour immunity via acylcarnitines, while palm oil fares better in obese mice!🧪 www.nature.com/articles/s42...

PLK1-mediated PDHA1 phosphorylation drives metabolic reprogramming in lung cancer - Oncogene Oncogene - PLK1-mediated PDHA1 phosphorylation drives metabolic reprogramming in lung cancer

More intriguing Promethion-powered research from Dr. X Liu & colleagues at University of Kentucky - PLK1 phosphorylation of PDHA1 rewires metabolism in lung cancer; DCA + onvansertib show synergy in mice! 🧪 www.nature.com/articles/s41...

Seasonal size change and aging in shrews

PhD Alert! 😍 Our lab is hiring a PhD student to study how shrews shrink in winter and grow in spring. Yes, you read that right!
tinyurl.com/shrinkingshr...
Join us at the @mpi-animalbehav.bsky.social, study a super cool animal, and join the @imprs-qbee.bsky.social community!

DM me for questions!

That expression... speaks volumes

"Now an extraordinarily successful scientific research system — one that took decades to build, has saved millions of lives and generated billions of dollars in profits for American companies and investors — is being dismantled before our eyes."

We are looking forward to hearing from Dr. Teresa Zimmers today in San Antonio.

Screenshot of the first page of the PDF of the Commentary, How can we best measure the energetic trade-offs faced by animals?, by Neil Metcalfe. The publishing information states: © 2025. Published by The Company of Biologists | Journal of Experimental Biology (2025) 228, jeb250303. doi:10.1242/jeb.250303. The first sentence of the Abstract reads: 'Energy is commonly presumed to be a limiting resource for most animals, forcing them to trade off the benefits of allocating energy to competing activities or processes'.

In his Commentary, Neil Metcalfe examines why it can be hard to detect trade-offs between two activities or processes competing for energy, despite energy supposedly being a limiting resource

journals.biologists.com/jeb/article/...

Well said.