Dr. Greeshma Shetty

So, you know, for in the trial, our patients were on a well-formulated ketogenic diet, which is very low carb. So 30 grams, um, but practically in our clinical workflows, We do a lot of low carb and not everybody's in well-formulated ketogenic diet. So we really try to sort of meet patients where they need to be. And there's a lot of heterogeneity in type two diabetes, right?

So, you know, for in the trial, our patients were on a well-formulated ketogenic diet, which is very low carb. So 30 grams, um, but practically in our clinical workflows, We do a lot of low carb and not everybody's in well-formulated ketogenic diet. So we really try to sort of meet patients where they need to be. And there's a lot of heterogeneity in type two diabetes, right?

So, you know, for in the trial, our patients were on a well-formulated ketogenic diet, which is very low carb. So 30 grams, um, but practically in our clinical workflows, We do a lot of low carb and not everybody's in well-formulated ketogenic diet. So we really try to sort of meet patients where they need to be. And there's a lot of heterogeneity in type two diabetes, right?

We've in genome wide association studies, we now know there's hundreds of different like types of type two diabetes, but sort of like the end result or the goal is to preserve beta cell functional mass, right? And the beta cells are those cells that make insulin. And so anything we can do to de-stress that beta cell and keep its insulin production up is critical. And when we eat high carb diets,

We've in genome wide association studies, we now know there's hundreds of different like types of type two diabetes, but sort of like the end result or the goal is to preserve beta cell functional mass, right? And the beta cells are those cells that make insulin. And so anything we can do to de-stress that beta cell and keep its insulin production up is critical. And when we eat high carb diets,

We've in genome wide association studies, we now know there's hundreds of different like types of type two diabetes, but sort of like the end result or the goal is to preserve beta cell functional mass, right? And the beta cells are those cells that make insulin. And so anything we can do to de-stress that beta cell and keep its insulin production up is critical. And when we eat high carb diets,

we add to cytokine release, inflammation, glucotoxicity, all of these things stress out the beta cell. And so that sort of accelerates the destruction of beta cell function and mass over time. And that's when you start seeing the one-way trolley for type 2 diabetes. So if you can reset that and change that pathway, you can definitely improve

we add to cytokine release, inflammation, glucotoxicity, all of these things stress out the beta cell. And so that sort of accelerates the destruction of beta cell function and mass over time. And that's when you start seeing the one-way trolley for type 2 diabetes. So if you can reset that and change that pathway, you can definitely improve

we add to cytokine release, inflammation, glucotoxicity, all of these things stress out the beta cell. And so that sort of accelerates the destruction of beta cell function and mass over time. And that's when you start seeing the one-way trolley for type 2 diabetes. So if you can reset that and change that pathway, you can definitely improve

insulin secretion and also decrease while you're losing weight, decrease the insulin resistance at other target organs like in your liver and your muscles. So you also spare the beta cell from having to produce more insulin to do the same job. So multiple layers of de-stressing the beta cell through the nutritional intervention directly, but also indirectly by affecting other parts of metabolism.

insulin secretion and also decrease while you're losing weight, decrease the insulin resistance at other target organs like in your liver and your muscles. So you also spare the beta cell from having to produce more insulin to do the same job. So multiple layers of de-stressing the beta cell through the nutritional intervention directly, but also indirectly by affecting other parts of metabolism.

insulin secretion and also decrease while you're losing weight, decrease the insulin resistance at other target organs like in your liver and your muscles. So you also spare the beta cell from having to produce more insulin to do the same job. So multiple layers of de-stressing the beta cell through the nutritional intervention directly, but also indirectly by affecting other parts of metabolism.

I mean, energy homeostasis is so complex. I have so much humility. You know, I started my fellowship training studying adipokines. I was in a lab where I was studying leptin and adiponectin. And like there are so many other cascades and they all interact with the gut, the microbiome, the brain, your satiety centers, your pancreas. So there's so much complexity.

I mean, energy homeostasis is so complex. I have so much humility. You know, I started my fellowship training studying adipokines. I was in a lab where I was studying leptin and adiponectin. And like there are so many other cascades and they all interact with the gut, the microbiome, the brain, your satiety centers, your pancreas. So there's so much complexity.

I mean, energy homeostasis is so complex. I have so much humility. You know, I started my fellowship training studying adipokines. I was in a lab where I was studying leptin and adiponectin. And like there are so many other cascades and they all interact with the gut, the microbiome, the brain, your satiety centers, your pancreas. So there's so much complexity.

So really thinking about it simplistically, though, is really preserving and de-stressing that beta cell.

So really thinking about it simplistically, though, is really preserving and de-stressing that beta cell.

So really thinking about it simplistically, though, is really preserving and de-stressing that beta cell.

Yeah. So when folks increase their fat intake and certainly when people achieve nutritional ketosis with higher ketone levels, the hormones that drive appetite are naturally suppressed and the hormones that signal satiety go up. So endogenous GLP-1, CCK go up and then things like ghrelin go down.

Yeah. So when folks increase their fat intake and certainly when people achieve nutritional ketosis with higher ketone levels, the hormones that drive appetite are naturally suppressed and the hormones that signal satiety go up. So endogenous GLP-1, CCK go up and then things like ghrelin go down.