SDRC MEMBER ACHIEVEMENTS: Katrin Svensson, PHD
Katrin Svensson, PhD
Associate Professor of Pathology
Katrin J. Svensson, PhD — Endocrine Society Early Career Investigator Award
Congratulations to Dr. Katrin J. Svensson on being named a recipient of the Richard E. Weitzman Outstanding Early Career Investigator Award from the Endocrine Society, which recognizes exceptionally promising young clinical or basic investigators. Dr. Svensson is an Associate Professor in the Department of Pathology at Stanford University and the Metabolic Core Director and Affinity Group Leader at the Stanford Diabetes Research Center. Her laboratory's pioneering work on intercellular communication and the discovery of novel secreted signaling molecules continues to advance our understanding of metabolic disease.
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SDRC Member Spotlight: Dr. Siddharth krishnan
Siddharth Krishnan, PhD
Assistant Professor of Electrical Engineering (and by courtesy, of Bioengineering and Materials Science and Engineering) | Stanford University SDRC Member since 2025 | Stanford Bio-X Affiliated Faculty
About Dr. Krishnan
Dr. Siddharth Krishnan's path to Stanford is one defined by curiosity, innovation, and a deep commitment to improving patient lives through technology. He earned both his BS and MS degrees from Washington University in St. Louis before completing his PhD at the University of Illinois at Urbana-Champaign under Professor John Rogers, where his doctoral thesis earned the Chakrapani Innovation Award for outstanding research.
Following his graduate training, Dr. Krishnan pursued postdoctoral work as a K99-funded Research Scientist in the laboratories of Professors Daniel Anderson and Robert Langer at the Koch Institute for Integrative Cancer Research at MIT and at Boston Children's Hospital — two of the most renowned research environments in biomedical engineering. It was during this period that he conducted the groundbreaking research on implantable islet cell devices featured below.
Dr. Krishnan joined Stanford University as an Assistant Professor of Electrical Engineering and Terman Faculty Fellow, and became a member of the Stanford Diabetes Research Center in 2025. His work sits at the intersection of bioelectronics, bioengineering, and therapeutic device development, and he has been recognized with numerous honors including a JDRF Postdoctoral Fellowship, the 2019 Illinois Innovation Prize, and a place on MIT Technology Review's prestigious Global Innovators Under 35 list. He is also co-founder of Rhaeos Inc., a company focused on translating his graduate research on wireless wearable diagnostic tools into clinical use for neurological surgery.
Dr. Krishnan is an active SDRC member and also received the 2026 SDRC Pilot & Feasibility Award.
Featured Publication
Implantable Islet Cells Could Control Diabetes Without Insulin Injections Research conducted at MIT & Boston Children's Hospital
For the millions of people living with Type 1 diabetes, daily life involves carefully monitoring blood sugar levels and administering multiple insulin injections — a demanding routine with a significant impact on quality of life. Dr. Krishnan, along with co-lead author Dr. Matthew Bochenek, set out to develop a transformative alternative.
Working at MIT prior to joining Stanford, Dr. Krishnan and colleagues engineered an implantable device containing insulin-producing pancreatic islet cells. The device addresses two of the most critical barriers to long-term success: it encapsulates the cells to protect them from immune rejection, and it incorporates an on-board oxygen generator to keep the cells healthy and functional over time.
In preclinical studies, the implanted islet cells survived for at least 90 days, remained functional, and produced sufficient insulin to regulate blood sugar levels in mice — a highly promising step toward a potential long-term alternative to daily insulin injections for Type 1 diabetes patients.
Connect with Dr. Krishnan
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SDRC Member Spotlight: Dr. Kyle Loh
SDRC member and Stanford Department of Developmental Biology faculty member Dr. Kyle Loh is fascinated by embryonic stem (ES) cell biology and the ability of ES cells to generate all of the cell types within the human body. However, getting ES cells to exclusively turn into a single cell type of therapeutic value, such as an insulin-producing pancreatic beta cell is immensely challenging. “How can we ‘force’ them to turn into a single kind of cell at the expense of other alternatives?”, muses Dr Loh. His group has made huge strides towards addressing this problem by delving deep into understanding the mechanisms underlying ES cell biology. Specifically, his work has systematically identified key molecular pathways controlling specific differentiation routes and has permitted the generation of nearly pure populations of therapeutically useful cell types such as liver cells and bone cells that could be transplanted into mouse models.
Our current understanding of ES cell biology points to a model where multiple factors and signaling pathways essentially keep ES cells in a state of ‘stemness’ or undifferentiation by suppressing differentiation into different cell types. Dr. Loh’s research has led him to challenge this prevailing view. He notes, “This is innately paradoxical to some degree, because a defining property of stem cells is their capacity to differentiate”. Instead, Dr. Loh proposed that the supposed ‘guardians’ of ES cell biology – the individual transcription factors that mark ES cells, may in fact promote differentiation to specific lineages while repressing alternative differentiation pathways. “Thus”, he argues, “co-expression of multiple such competing transcription factors would engender a ‘precarious balance’ whereby multiple downstream lineage options are simultaneously poised but the stem cell does not differentiate into any of them”.
Dr. Loh’s work has provided a road map that allows researchers to nudge ES cells along their differentiation pathway of choice to generate a pure population of therapeutically useful cells. However, he notes that significant challenges remain. “A pure batch of cells is not an organ, and for certain types of cell replacement therapies, it may be necessary to transplant complex constructs comprised of multiple cell types”, he explains.
Another challenge that Dr. Loh is addressing is to ensure that transplanted cells are not rejected by patient immune systems. Immune rejection is a major roadblock for type 1 diabetic patients whose immune systems are programmed to attack not just their own beta cells but also transplanted islet cells. Dr. Loh conducted preclinical animal studies in collaboration with other SDRC members to deplete the host blood system and replace it with healthy donor blood cells through a process known as ‘conditioning’. Dr. Loh anticipates that similar approaches will be instrumental in safely replacing a patient’s immune system and inducing tolerance to transplanted cells.
Dr. Loh’s group is a part of the recently established Juvenile Diabetes Research Foundation (JDRF) Northern California Center of Excellence (COE) to develop cell replacement therapies for type 1 diabetes. The COE comprises a team of investigators from Stanford and the University of California at San Francisco and supported by the SDRC resources and expertise. Speaking about his research partnerships with other SDRC scientists including Drs. Seung Kim and Judith Shizuru to develop regenerative therapies for type 1 diabetes, Dr. Loh says, “It has been great to be part of a well-integrated diabetes research community”.
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SDRC Member Spotlight: A conversation with Jon Long
Dr Jon Long, an SDRC member and assistant professor of pathology at the Stanford School of Medicine is deeply interested in energy metabolism. He joined Stanford in January 2018 after completing his postdoctoral training at the Dana Farber Cancer Institute, Harvard Medical School. His lab focuses on mechanisms that control mammalian energy homeostasis with an emphasis on discovering new small molecules and pathways that regulate metabolism and physiology.
Dr Long recently presented research from his laboratory at the weekly SDRC member meeting uncovering a new metabolite implicated in energy homeostasis. His work identified a natural molecular pathway that drives cells to burn calories instead of storing them as fat, essentially inducing weight loss. It could have potential implications in treating obesity and other metabolic disorders.
Dr Long has ongoing collaborations and interactions with other SDRC members including Dr Joshua Knowles and Dr Carolyn Bertozzi. Here, he talks about how he became interested in energy metabolism, his work and his philosophy towards understanding and treating metabolic disorders.
You study pathways controlling mammalian energy homeostasis. What initially drove you to focus on this topic?
Every day, we each encounter a wide array of different energy states, depending on our last meal, our current activity levels, or the environmental temperature, just to name a few variables. How do we sense changes in our energy states, and what are the mechanisms that we use to respond and maintain energy balance? I’ve been attracted to this problem because energy metabolism is a universal process that we have all experienced.
How do you think about the problem of obesity and its related diseases like diabetes in the context of energy homeostasis?
The first law of thermodynamics says that energy cannot be made or destroyed, only converted. This law also applies to organismal energy metabolism. This means that counteracting obesity and its associated metabolic disorders like diabetes requires either a reduction of energy input or an increase in energy expenditure. So far, there is nothing available to increase energy expenditure in people. That seemed to me like an interesting arm that one could manipulate at a molecular level in specific ways to augment energy output and reduce obesity and metabolic disease.
Your group identified a new class of metabolites, N-acyl amino acids, which essentially promote energy expenditure and weight loss in mice. What led to this discovery?
The main discovery that I made during my postdoc and what my research at Stanford is based on is a family of circulating “anti-obesity” molecules in the body called N-acyl amino acids. We found that they directly stimulate mitochondria to increase mitochondrial respiration and increase energy expenditure. Our path to discovering these molecules started because we were studying an enzyme called PM20D1. Mice overexpressing PM20D1 exhibited a hypermetabolism through an unknown mechanism. We found that PM20D1 does this by catalyzing the formation of N-acyl amino acids from lipids and amino acids, and worked out from there the mechanism by which N-acyl amino acids stimulate respiration.
Obesity and diabetes are such complex diseases. Do you think that targeting metabolic homeostasis alone would be enough as a therapeutic strategy to solve the underlying problems in these diseases?
The increase in obesity and metabolic disorders is a very complex process with many underlying causes that range from socio-economic, environmental and genetic. Potential pharmacological intervention is just one of several strategies by which these diseases need to be addressed. I see our work as one small part of societal efforts to combat this constellation of disorders.
Does this mean we can finally eat whatever we want and still lose weight? How do you address all the science myths and fads around weight loss as a scientist?
Unfortunately for most of us, I don’t think there will ever be a day when we can eat whatever we want. I see it as my responsibility, through interviews like these, to explain as accurately as I can and from a scientific view, the pathways regulating energy metabolism and weight loss. As for the other myths and fads, all I can say is that I don’t pay attention but instead try to follow the standard medical advice- I try to eat a well-balanced diet and get some exercise.
How do you envision your research contributing towards therapy to combat diabetes and obesity?
One of the long-term goals of my research is to identify and understand new molecules and pathways that control energy expenditure. It would be my dream that we might be able to therapeutically exploit these energy expenditure pathways to develop new drugs that could reduce obesity in people. A better understanding about how N-acyl amino acids work might enable such a discovery.
How has the SDRC contributed to your research as a junior investigator?
The SDRC is a fantastic group of incredibly diverse scientists. Investigators come from endocrinology, or stem cells, or genetics, or engineering, or immunology, or developmental biology, just to name a few fields. This diversity of approaches has really served as a wonderful springboard for thinking about new ideas.
To learn more about Dr Long’s research, please visit https://longlabstanford.org/
By
Harini Chakravarthy
Harini Chakravarthy is a science writer for the Stanford Diabetes Research Center.