DR. KENNETH S. POLONSKY, MD

SAINT LOUIS, MO

Research Active
Internal Medicine - Endocrinology, Diabetes & Metabolism NPI registered 20+ years 50 publications 2005 – 2016 NPI: 1275559585

Practice Location

660 S EUCLID AVE
SAINT LOUIS, MO 63110-1010

Phone: (314) 362-3500

What does KENNETH POLONSKY research?

Kenneth S Polonsky studies how certain hormones and genes affect the body's ability to manage blood sugar, especially in the context of diabetes. One major area of his research is the gut hormone xenin-25, which has shown promise in delaying stomach emptying and lowering blood sugar after meals in both healthy individuals and those with type 2 diabetes. He also investigates the role of a protein called HNF-1alpha, which regulates the growth of insulin-producing cells in the pancreas. Understanding these processes is crucial for developing new treatments for diabetes and conditions related to blood sugar management.

Key findings

  • Xenin-25 infusion for at least 90 minutes significantly slows gastric emptying and reduces post-meal blood sugar levels across individuals with normal glucose tolerance, prediabetes, and type 2 diabetes.
  • Genetically modified mice lacking normal HNF-1alpha had a reduced ability to grow insulin-producing pancreatic cells, leading to higher blood sugar levels, demonstrating the protein's critical control over pancreatic cell growth.
  • The study on HNF-1alpha revealed that it regulates multiple genes affecting cell growth, which helps explain how mutations can lead to a form of inherited diabetes known as MODY3.

Frequently asked questions

Does Dr. Polonsky study diabetes?
Yes, Dr. Polonsky's work focuses extensively on diabetes, particularly on how certain hormones and genetic factors influence insulin production and blood sugar levels.
What treatments has Dr. Polonsky researched?
He has researched the effects of xenin-25 on slowing stomach emptying and reducing blood sugar levels, indicating its potential for diabetes management.
Is Dr. Polonsky's work relevant to type 2 diabetes?
Yes, his research on xenin-25 and insulin-producing cells directly relates to both type 2 diabetes and glucose management strategies.

Publications in plain English

Pancreatic β-Cell Death due to Pdx-1 Deficiency Requires Multi-BH Domain Protein Bax but Not Bak.

2016

The Journal of biological chemistry

Sun J, Mao LQ, Polonsky KS, Ren DC

Plain English
This study looked at how a specific protein, called Pdx1, affects the death of insulin-producing cells in the pancreas, which can lead to diabetes. Researchers found that when Pdx1 is low, a protein named Bax contributes to the death of these cells, and blocking Bax increased the number of healthy insulin-producing cells and improved blood sugar control in mice. This matters because it helps identify a potential target for diabetes treatment by preventing cell death in the pancreas. Who this helps: Patients with diabetes.

PubMed

Donald F. Steiner MD, 1930-2014: discoverer of proinsulin.

2015

Proceedings of the National Academy of Sciences of the United States of America

Philipson LH, Bell G, Polonsky KS

PubMed

Donald F. Steiner, MD, 1930-2014: pioneering diabetes researcher.

2015

Diabetologia

Polonsky KS, Rubenstein AH

PubMed

Research in academic medical centers: two threats to sustainable support.

2015

Science translational medicine

Levine AS, Alpern RJ, Andrews NC, Antman K, Balser JR +14 more

Plain English
This study looked at how cuts in federal funding and income from patient care are putting biomedical research at risk, which can also affect medical practices and patient care. The findings indicate that less financial support could harm the quality and progress of medical research. This matters because without sufficient funding, we may see fewer advancements in treatments and overall healthcare improvement. Who this helps: This helps patients and healthcare providers.

PubMed

β-cell failure in type 2 diabetes: postulated mechanisms and prospects for prevention and treatment.

2014

The Journal of clinical endocrinology and metabolism

Halban PA, Polonsky KS, Bowden DW, Hawkins MA, Ling C +5 more

Plain English
This research paper looks at how the failure of insulin-producing cells, known as β-cells, contributes to type 2 diabetes (T2D) and explores ways to better prevent and treat this condition. The authors discussed the genetic factors that might influence β-cell failure and emphasized the need for improved tests and therapies that focus on enhancing β-cell function and increasing their numbers. They highlighted several key goals for future research, such as understanding the genetics behind T2D and finding new ways to support β-cells through therapies. Who this helps: This helps patients with type 2 diabetes and their doctors by providing insights for better treatment options.

PubMed

BH3-only molecule Bim mediates β-cell death in IRS2 deficiency.

2014

Diabetes

Ren D, Sun J, Mao L, Ye H, Polonsky KS

Plain English
Researchers studied a specific protein called Bim, which contributes to the death of insulin-producing cells (beta-cells) when a gene known as IRS2 is lacking. They found that when they reduced IRS2, it led to increased levels of Bim and more beta-cell death. Specifically, in tests with mice missing the IRS2 gene, removing Bim helped restore beta-cell numbers and improved their ability to manage blood sugar levels. Who this helps: This research benefits patients with type 2 diabetes and may help doctors find new ways to protect insulin-producing cells.

PubMed

β-cell failure in type 2 diabetes: postulated mechanisms and prospects for prevention and treatment.

2014

Diabetes care

Halban PA, Polonsky KS, Bowden DW, Hawkins MA, Ling C +5 more

Plain English
This research paper focuses on the failure of β-cells, which are crucial for insulin production, in people with type 2 diabetes (T2D). It highlights that β-cell failure is a key factor in the onset and worsening of the disease and suggests that genetic reasons play a role. The paper emphasizes the need for future research to better understand these mechanisms and find new ways to prevent and treat T2D, including improving β-cell function and exploring new cell-based treatments. Who this helps: This helps patients with type 2 diabetes and their doctors by providing insights for better management and treatment options.

PubMed

Role of BH3-only molecules Bim and Puma in β-cell death in Pdx1 deficiency.

2014

Diabetes

Ren D, Sun J, Wang C, Ye H, Mao L +3 more

Plain English
Researchers studied the connection between a gene called PDX1, which helps regulate insulin production in the pancreas, and the death of insulin-producing cells (β-cells) in mice that developed diabetes due to PDX1 deficiency. They found that when they removed two specific proteins, Bim and Puma, from these mice, the mice had better blood sugar levels, more insulin-producing cells, and fewer dying cells. This is important because it highlights a potential way to protect insulin-producing cells and improve diabetes management. Who this helps: This helps patients with diabetes and their doctors.

PubMed

Xenin-25 delays gastric emptying and reduces postprandial glucose levels in humans with and without type 2 diabetes.

2014

American journal of physiology. Gastrointestinal and liver physiology

Chowdhury S, Reeds DN, Crimmins DL, Patterson BW, Laciny E +9 more

Plain English
Infusing the gut hormone xenin-25 slowed stomach emptying and reduced after-meal blood glucose in people with normal glucose tolerance, prediabetes, and type 2 diabetes equally, but only when the infusion lasted at least 90 minutes. The hormone worked by activating nerve pathways to the stomach rather than by directly stimulating insulin release. These findings suggest xenin-25 could be a target for therapies that slow glucose absorption after meals.

PubMed

Complex patterns of metabolic and Ca²⁺ entrainment in pancreatic islets by oscillatory glucose.

2013

Biophysical journal

Pedersen MG, Mosekilde E, Polonsky KS, Luciani DS

Plain English
This study looked at how fluctuating glucose levels affect insulin secretion and electrical activity in clusters of cells (islets) in the pancreas. The researchers found that these glucose changes can create different patterns of activity in the islets, specifically showing that one part of the islet can sync with another part, sometimes in a one-to-one or one-to-two rhythm. This is important because it shows how the pancreas might coordinate its insulin release more effectively, which can help manage blood sugar levels. Who this helps: This helps patients with diabetes by potentially improving how doctors can manage insulin secretion.

PubMed

Moderate effect of duodenal-jejunal bypass surgery on glucose homeostasis in patients with type 2 diabetes.

2012

Obesity (Silver Spring, Md.)

Klein S, Fabbrini E, Patterson BW, Polonsky KS, Schiavon CA +4 more

Plain English
This study looked at the effects of a specific type of surgery, called duodenal-jejunal bypass (DJB), on blood sugar control in overweight adults with type 2 diabetes. After the surgery, participants lost weight and their average blood sugar levels, measured by glycated hemoglobin, dropped from 9.3% to 7.7% over 12 months. Additionally, about 20% of participants no longer needed diabetes medications and achieved normal blood sugar levels. Who this helps: This benefits patients with type 2 diabetes who are struggling to manage their condition.

PubMed

Xenin-25 amplifies GIP-mediated insulin secretion in humans with normal and impaired glucose tolerance but not type 2 diabetes.

2012

Diabetes

Wice BM, Reeds DN, Tran HD, Crimmins DL, Patterson BW +5 more

Plain English
This study investigated how a substance called xenin-25 influences insulin secretion in humans with different levels of glucose tolerance: normal, impaired, and type 2 diabetes (T2DM). Researchers found that while xenin-25 and GIP together improved insulin secretion in people with normal and impaired glucose tolerance, they had no effect on those with T2DM. This matters because understanding how xenin-25 works may help develop treatments for glucose management in individuals with prediabetes or normal glucose levels, though it is not effective for those with T2DM. Who this helps: Patients with normal or impaired glucose tolerance.

PubMed

Ginsenoside Re rapidly reverses insulin resistance in muscles of high-fat diet fed rats.

2012

Metabolism: clinical and experimental

Han DH, Kim SH, Higashida K, Jung SR, Polonsky KS +2 more

Plain English
Researchers studied the effects of a substance called ginsenoside Re from ginseng berries on insulin resistance in rats that were fed a high-fat diet. They found that after just 90 minutes of treatment, ginsenoside Re completely restored the rats' ability to transport glucose in their muscles, which had been reduced by about 50% due to the high-fat diet. This finding is important because improving insulin response can help in managing conditions like diabetes and obesity. Who this helps: This helps patients struggling with insulin resistance, especially those with obesity or diabetes.

PubMed

The past 200 years in diabetes.

2012

The New England journal of medicine

Polonsky KS

PubMed

Introduction of Arthur H. Rubenstein.

2012

The Journal of clinical investigation

Polonsky KS

PubMed

Ginseng and ginsenoside Re do not improve β-cell function or insulin sensitivity in overweight and obese subjects with impaired glucose tolerance or diabetes.

2011

Diabetes care

Reeds DN, Patterson BW, Okunade A, Holloszy JO, Polonsky KS +1 more

Plain English
This study looked at whether ginseng and its active component, ginsenoside Re, could help improve insulin function in overweight or obese people with early signs of diabetes. After 30 days of taking these supplements, the researchers found no significant improvement in insulin sensitivity or β-cell function; for instance, the β-cell function in the ginseng group decreased slightly from 7.7 to 6.0, but this was not considered significant. These findings are important because they suggest that ginseng may not be effective for treating insulin resistance in these patients, possibly due to the body not absorbing these substances well. Who this helps: This information benefits patients with diabetes and healthcare providers seeking effective treatments.

PubMed

TCF7L2 variant rs7903146 affects the risk of type 2 diabetes by modulating incretin action.

2010

Diabetes

Villareal DT, Robertson H, Bell GI, Patterson BW, Tran H +2 more

Plain English
This study looked at how a specific genetic variant (TCF7L2 variant rs7903146) influences the risk of developing type 2 diabetes by affecting how the body responds to incretin hormones, which help regulate insulin secretion. Researchers found that people with this genetic variant had 50% lower insulin response to oral glucose compared to those without it and a 30% lower incretin effect, even though hormone levels were similar between both groups. Understanding this connection is important because it highlights potential treatment strategies that could improve incretin sensitivity and reduce the risk of type 2 diabetes. Who this helps: This helps patients at risk for type 2 diabetes.

PubMed

Calpain-10 is a component of the obesity-related quantitative trait locus Adip1.

2010

Journal of lipid research

Cheverud JM, Fawcett GL, Jarvis JP, Norgard EA, Pavlicev M +5 more

Plain English
This study looked at a gene called calpain-10 and its connection to obesity and related health issues in mice. Researchers found that mice with a version of the calpain-10 gene that was disabled (Capn10 knockout) gained more weight and had higher levels of certain fats in their blood, particularly when crossed with one specific type of mouse (LG/J), but not with another type (SM/J). Understanding how this gene affects weight and diabetes is important because it could lead to better ways to treat or prevent these conditions in people. Who this helps: This helps researchers and doctors working on obesity and diabetes treatments.

PubMed

Xenin-25 potentiates glucose-dependent insulinotropic polypeptide action via a novel cholinergic relay mechanism.

2010

The Journal of biological chemistry

Wice BM, Wang S, Crimmins DL, Diggs-Andrews KA, Althage MC +8 more

Plain English
This study looked at how a substance called xenin-25 affects insulin release in mice that struggle to respond to a hormone called GIP, which is important for managing blood sugar levels. Researchers found that while the mice normally didn't respond well to GIP, treating them with xenin-25 improved their insulin release and helped lower their high blood sugar levels; specifically, it restored GIP's effect, although xenin-25 alone didn’t have this effect. This is important because it points to a new way to treat type 2 diabetes by improving the body's response to GIP, which could lead to better blood sugar control for patients. Who this helps: Patients with type 2 diabetes.

PubMed

Targeting cyclophilin D and the mitochondrial permeability transition enhances beta-cell survival and prevents diabetes in Pdx1 deficiency.

2010

Proceedings of the National Academy of Sciences of the United States of America

Fujimoto K, Chen Y, Polonsky KS, Dorn GW

Plain English
This research studied how a genetic mutation affecting the Pdx1 gene leads to the death of insulin-producing beta-cells in the pancreas, which is a key factor in the development of diabetes. The researchers found that blocking a specific protein called cyclophilin D helped protect these beta-cells, improving their survival and restoring normal blood sugar levels in mice. This is important because it points to a potential treatment target for preventing diabetes in individuals with Pdx1 gene mutations. Who this helps: This helps patients with heritable diabetes linked to Pdx1 gene mutations.

PubMed

Loss of Nix in Pdx1-deficient mice prevents apoptotic and necrotic β cell death and diabetes.

2010

The Journal of clinical investigation

Fujimoto K, Ford EL, Tran H, Wice BM, Crosby SD +2 more

Plain English
This study looked at how a protein called Nix affects the death of insulin-producing beta cells in mice with a mutation linked to type 2 diabetes. Researchers found that when Nix was blocked in these mice, their beta cell numbers and insulin production returned to normal, preventing high blood sugar levels after eating. This is important because it shows that targeting Nix could be a way to protect beta cells and manage diabetes. Who this helps: This helps patients with type 2 diabetes and their doctors by identifying a new potential target for treatment.

PubMed

The physician scientist training program in internal medicine at Washington University School of Medicine.

2009

Academic medicine : journal of the Association of American Medical Colleges

Muslin AJ, Kornfeld S, Polonsky KS

Plain English
The research focused on a training program for physician scientists at Washington University School of Medicine, which blends medical training and research skills to better prepare doctors for academic roles. Since its launch in 2000, the Physician Scientist Training Program (PSTP) has structured the path from completing MD-PhD degrees to becoming faculty members, ensuring these professionals receive specialized training in internal medicine or dermatology along with research opportunities. This matters because it helps create skilled medical professionals who can translate research findings into better patient care and innovative treatments. Who this helps: This primarily benefits medical students and professionals aiming to balance clinical practice with research careers.

PubMed

Insulin signaling in alpha cells modulates glucagon secretion in vivo.

2009

Cell metabolism

Kawamori D, Kurpad AJ, Hu J, Liew CW, Shih JL +5 more

Plain English
This study looked at how insulin affects glucagon secretion in specific cells called alpha cells, using specially designed mice that lack insulin receptors in these cells. The researchers found that these mice had high levels of glucose and glucagon, especially after eating and when faced with low blood sugar. This research is important because it shows that insulin signaling in alpha cells plays a critical role in managing blood sugar levels, which could help in understanding diabetes better. Who this helps: This helps patients with diabetes by providing insights into better management of their blood sugar levels.

PubMed

Serum leptin levels in obese males during over- and underfeeding.

2009

Obesity (Silver Spring, Md.)

Cooper JA, Polonsky KS, Schoeller DA

Plain English
This study looked at how the hormone leptin, which helps regulate hunger and energy balance, changes in response to eating more or less food in obese men. Researchers found that when these men ate less (underfeeding), leptin levels dropped by about 21%, and when they ate more (overfeeding) after previously eating less, leptin levels rose by 25%. However, if they ate more without having been underfed first, their leptin levels barely changed. This is important because it shows that leptin in obese men doesn’t react to eating more food in a way that helps control weight, which could contribute to ongoing weight gain. Who this helps: This research helps doctors and health professionals understand the metabolic differences in obese patients.

PubMed

To nap or not to nap? Residents' work hours revisited.

2009

The New England journal of medicine

Blanchard MS, Meltzer D, Polonsky KS

PubMed

Kir6.2 variant E23K increases ATP-sensitive K+ channel activity and is associated with impaired insulin release and enhanced insulin sensitivity in adults with normal glucose tolerance.

2009

Diabetes

Villareal DT, Koster JC, Robertson H, Akrouh A, Miyake K +4 more

Plain English
This study looked at a genetic variation called E23K in a protein that controls potassium channels related to insulin release. Researchers found that people with the E23K variant had 40% lower insulin secretion when given glucose but also had about 40% enhanced sensitivity to insulin, allowing them to maintain normal blood sugar levels despite the reduced insulin. This matters because it helps explain why some people may be at a higher risk for type 2 diabetes over time, as their insulin production can weaken. Who this helps: This helps patients at risk for type 2 diabetes and their doctors in understanding their condition better.

PubMed

Autophagy regulates pancreatic beta cell death in response to Pdx1 deficiency and nutrient deprivation.

2009

The Journal of biological chemistry

Fujimoto K, Hanson PT, Tran H, Ford EL, Han Z +5 more

Plain English
This study looked at how a process called autophagy affects the death of pancreatic cells that produce insulin, especially when there's a lack of a specific protein (Pdx1) and during starvation. Researchers found that increased autophagy was linked to more beta cell death in mice with lower Pdx1 levels, and preventing autophagy helped keep these cells alive longer. This research shows that targeting autophagy might be a new way to protect insulin-producing cells and improve diabetes treatment. Who this helps: This helps patients with diabetes and their doctors.

PubMed

Variation in the perilipin gene (PLIN) affects glucose and lipid metabolism in non-Hispanic white women with and without polycystic ovary syndrome.

2009

Diabetes research and clinical practice

Kawai T, Ng MC, Hayes MG, Yoshiuchi I, Tsuchiya T +5 more

Plain English
This study looked at how variations in the perilipin gene (PLIN) impact blood sugar and fat levels in white women, focusing on those with polycystic ovary syndrome (PCOS) and those without it. Researchers found that one specific genetic variation increased the risk of glucose intolerance by about 75% in women without PCOS and 67% in those with PCOS. It also led to higher levels of bad cholesterol (LDL) and total cholesterol, highlighting a connection between this gene and metabolic health issues. Who this helps: This helps women with or at risk for PCOS, as well as their doctors in managing metabolic health.

PubMed

Pdx1 and other factors that regulate pancreatic beta-cell survival.

2009

Diabetes, obesity & metabolism

Fujimoto K, Polonsky KS

Plain English
This study looked at a protein called Pdx1, which is important for the health and survival of cells in the pancreas that produce insulin. Researchers found that when Pdx1 levels drop, it leads to more cell death and worsens diabetes; for example, a complete lack of Pdx1 results in no pancreas at all, while lower levels contribute to serious problems in insulin-producing cells. Understanding how Pdx1 relates to these cell deaths is crucial for creating better ways to prevent and treat diabetes. Who this helps: This research benefits patients with diabetes and those at risk of developing the disease.

PubMed

Impaired insulin secretion in transgenic mice over-expressing calpastatin in pancreatic β-cells.

2009

Islets

Johnson JD, Otani K, Bell GI, Polonsky KS

Plain English
This research studied how a protein called calpastatin affects insulin secretion in mice that were genetically modified to express it in their insulin-producing cells. The findings showed that these modified mice had higher blood sugar levels and released less insulin when exposed to high glucose, indicating a problem with their insulin response; specifically, their insulin-producing cells released too much insulin at low glucose levels but struggled to respond properly at high glucose levels. This is important because it shows that disrupting the normal function of calpains can impair insulin secretion, which is key to understanding diabetes better. Who this helps: This helps researchers and doctors working on treatments for type 2 diabetes.

PubMed

Role of HNF-1alpha in regulating the expression of genes involved in cellular growth and proliferation in pancreatic beta-cells.

2009

Diabetes research and clinical practice

Uchizono Y, Baldwin AC, Sakuma H, Pugh W, Polonsky KS +1 more

Plain English
Researchers created genetically modified mice to study how a protein called HNF-1alpha controls the growth of insulin-producing cells in the pancreas—the same protein that malfunctions in people with a form of inherited diabetes (MODY3). They found that mice lacking normal HNF-1alpha couldn't grow enough of these insulin-producing cells and had higher blood sugar levels as a result. The study reveals that HNF-1alpha controls multiple genes that tell pancreatic cells when to grow and multiply, explaining why mutations in this protein cause diabetes in humans.

PubMed

Weight loss therapy improves pancreatic endocrine function in obese older adults.

2008

Obesity (Silver Spring, Md.)

Villareal DT, Banks MR, Patterson BW, Polonsky KS, Klein S

Plain English
This study looked at how weight loss therapy affects the pancreas and insulin sensitivity in obese older adults. After 6 months, participants who followed a diet and exercise program lost about 9% of their body weight and doubled their insulin sensitivity, while those who did not change their lifestyle saw no improvements. These changes in weight and insulin response may help lower the risk of developing type 2 diabetes in older adults. Who this helps: This helps obese older adults at risk for type 2 diabetes.

PubMed

Targeted ablation of glucose-dependent insulinotropic polypeptide-producing cells in transgenic mice reduces obesity and insulin resistance induced by a high fat diet.

2008

The Journal of biological chemistry

Althage MC, Ford EL, Wang S, Tso P, Polonsky KS +1 more

Plain English
This research studied special cells in the intestines that produce hormones affecting weight and blood sugar levels, specifically the hormone GIP. By reducing the number of these cells in mice, researchers found that the mice lost 25% of their body weight, had 77% lower levels of a hormone related to fat storage (leptin), ate 16% less, and were 10% more efficient in using energy, all while maintaining stable blood sugar levels. This matters because it shows a potential way to combat obesity and insulin resistance, conditions that lead to diabetes. Who this helps: This helps patients struggling with obesity and insulin resistance, as well as doctors looking for new treatment strategies.

PubMed

Standardization of C-peptide measurements.

2008

Clinical chemistry

Little RR, Rohlfing CL, Tennill AL, Madsen RW, Polonsky KS +5 more

Plain English
This study looked at how different labs measure C-peptide, a substance that shows how much insulin the body is producing in diabetic patients. They found that these measurements varied widely between labs, with differences sometimes exceeding 10%. However, by using a standardized reference method, they were able to significantly improve the consistency of these results, meaning that after standardization, labs were more likely to report similar C-peptide levels. Who this helps: This benefits patients and doctors by ensuring more accurate C-peptide testing, leading to better diabetes management.

PubMed

Carboxypeptidase E mediates palmitate-induced beta-cell ER stress and apoptosis.

2008

Proceedings of the National Academy of Sciences of the United States of America

Jeffrey KD, Alejandro EU, Luciani DS, Kalynyak TB, Hu X +5 more

Plain English
This study investigated how a fatty acid called palmitate affects the health of insulin-producing cells in the pancreas, known as beta-cells, which are crucial for controlling blood sugar levels. Researchers found that palmitate decreases a protein called carboxypeptidase E (CPE), leading to stress in the cells and eventually causing them to die. Specifically, reducing CPE levels by about 30% increased cell stress and death, while increasing CPE helped protect the cells from damage caused by palmitate. Who this helps: This research benefits patients with type 2 diabetes by highlighting potential targets for new treatments that could protect beta-cells.

PubMed

Gastric banding to treat obesity: band-aid or breakthrough?

2008

Nature clinical practice. Endocrinology & metabolism

Polonsky KS, Klein S

PubMed

International comparison of C-peptide measurements.

2007

Clinical chemistry

Wiedmeyer HM, Polonsky KS, Myers GL, Little RR, Greenbaum CJ +2 more

Plain English
This study looked at how well different laboratories and methods measure C-peptide, a marker for insulin production in diabetes patients. Researchers sent out samples to 15 labs in 7 countries and found that results varied significantly, especially at higher C-peptide levels. Using samples for calibration improved agreement between labs, making results more reliable. Who this helps: This benefits diabetes patients who need accurate monitoring of their insulin levels.

PubMed

Sustained expression of hepatocyte nuclear factor-6 leads to loss of pancreatic beta-cells by apoptosis.

2007

Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association

Hara M, Shen J, Pugh W, Polonsky KS, Le Beau MM +1 more

Plain English
This study looked at the role of a protein called HNF-6 in pancreatic beta-cells, which produce insulin. The researchers created mice that had high levels of HNF-6 and found that, by six weeks of age, these mice lost about 30% of their beta-cells due to a process called programmed cell death, also known as apoptosis. These findings are important because they suggest that high levels of HNF-6 might contribute to problems with insulin production, which is a key issue in diabetes. Who this helps: This helps doctors and researchers studying diabetes and finding new treatments.

PubMed

Ca2+ controls slow NAD(P)H oscillations in glucose-stimulated mouse pancreatic islets.

2006

The Journal of physiology

Luciani DS, Misler S, Polonsky KS

Plain English
This study looked at how calcium levels affect the way pancreatic cells release insulin in a fluctuating pattern when exposed to glucose. Researchers found that in about 90% of the mouse pancreatic cells tested, there were slow changes in a substance called NAD(P)H, which reflected the calcium levels, occurring every five minutes. This is important because understanding these processes could help improve treatments for diabetes by providing insights into how insulin secretion works. Who this helps: This helps patients with diabetes and the doctors treating them.

PubMed

Inhibition of calpain results in impaired contraction-stimulated GLUT4 translocation in skeletal muscle.

2006

American journal of physiology. Endocrinology and metabolism

Otani K, Polonsky KS, Holloszy JO, Han DH

Plain English
The study examined how blocking a protein called calpain affects glucose transport in muscle cells by focusing on a specific protein, GLUT4, that helps move glucose into the cells. Researchers found that while mice with less calpain had about three times more GLUT4 and other proteins involved in muscle activity, they still did not see any improvement in how effectively glucose was transported into the muscles when the muscles contracted. This is important because it shows that merely increasing GLUT4 isn't enough for better glucose uptake; there are additional barriers that need to be addressed for muscle function and glucose regulation. Who this helps: This research benefits patients with insulin resistance, particularly those with type 2 diabetes.

PubMed

Retinol-binding protein 4, insulin resistance, and type 2 diabetes.

2006

The New England journal of medicine

Polonsky KS

PubMed

A significant role for histocompatibility in human islet transplantation.

2006

Transplantation

Mohanakumar T, Narayanan K, Desai N, Ramachandran S, Shenoy S +9 more

Plain English
This study looked at how the body's reaction to certain proteins, called histocompatibility antigens, affects the success of islet transplants for people with type 1 diabetes. Researchers analyzed data from seven patients and found that those who were sensitized to the donor's antigens before or after the transplant experienced more failures; specifically, there was a strong link between this sensitization and the rejection of the transplanted cells. Understanding this relationship is important for selecting patients who are more likely to succeed with islet transplants, possibly improving overall outcomes. Who this helps: This helps patients with type 1 diabetes who are considering islet transplantation.

PubMed

Suppressed insulin signaling and increased apoptosis in CD38-null islets.

2006

Diabetes

Johnson JD, Ford EL, Bernal-Mizrachi E, Kusser KL, Luciani DS +5 more

Plain English
This study looked at the role of a protein called CD38 in insulin-producing cells in the pancreas. Researchers found that when CD38 was absent, these cells were more likely to die, with 27% greater apoptosis observed, and they didn’t respond well to insulin, highlighting that CD38 helps protect these cells and maintain their function. However, the absence of CD38 didn't significantly affect blood sugar control in the mice tested. Who this helps: This helps researchers and doctors understand diabetes mechanisms better, potentially aiding in developing new treatments.

PubMed

International trial of the Edmonton protocol for islet transplantation.

2006

The New England journal of medicine

Shapiro AM, Ricordi C, Hering BJ, Auchincloss H, Lindblad R +26 more

Plain English
This study looked at islet transplantation as a treatment for people with type 1 diabetes who struggle with severe low blood sugar. Researchers enrolled 36 participants and found that 44% maintained insulin independence and good blood sugar control one year after transplantation. However, by the two-year mark, most of these participants needed insulin again, indicating that while the procedure can help, the benefits may not last long-term. Who this helps: This research benefits patients with type 1 diabetes who experience severe hypoglycemia.

PubMed

Insulin protects islets from apoptosis via Pdx1 and specific changes in the human islet proteome.

2006

Proceedings of the National Academy of Sciences of the United States of America

Johnson JD, Bernal-Mizrachi E, Alejandro EU, Han Z, Kalynyak TB +7 more

Plain English
This study looked at how insulin helps protect pancreatic beta cells from dying under stress. Researchers found that low doses of insulin completely stopped these cells from dying, while higher doses did not have this effect. They also discovered that insulin works by activating a protein called Pdx1, which is crucial for cell survival. This is important because it shows that controlling insulin levels can help preserve the function of these important cells in the pancreas, which is vital for diabetes treatment. Who this helps: This research benefits patients with diabetes by providing insights into treatments that protect their pancreatic function.

PubMed

Reduced expression of the insulin receptor in mouse insulinoma (MIN6) cells reveals multiple roles of insulin signaling in gene expression, proliferation, insulin content, and secretion.

2005

The Journal of biological chemistry

Ohsugi M, Cras-Méneur C, Zhou Y, Bernal-Mizrachi E, Johnson JD +3 more

Plain English
This study looked at how reducing the amount of insulin receptors in mouse insulinoma cells affects various cellular functions. By lowering insulin receptor levels by up to 80%, the researchers found that the cells not only had trouble responding to insulin, but also showed changes in over 1,500 genes, experienced slower growth, and produced less insulin. These findings highlight the crucial role of insulin signaling in maintaining healthy beta cell functions, which could help in understanding diabetes better. Who this helps: This helps researchers and doctors working to find new treatments for diabetes.

PubMed

Insulin sensitivity by oral glucose minimal models: validation against clamp.

2005

American journal of physiology. Endocrinology and metabolism

Dalla Man C, Yarasheski KE, Caumo A, Robertson H, Toffolo G +2 more

Plain English
This study tested two new methods for measuring how well the body responds to insulin using oral tests, specifically during a glucose drink test. The researchers found that while one method showed lower insulin sensitivity than the traditional gold standard (13.66 vs. 8.08), the other method closely matched it (8.84 vs. 8.17), which means it can reliably estimate insulin sensitivity. This is important because it may provide a simpler way to assess insulin sensitivity in larger clinical studies, helping to identify issues related to conditions like diabetes. Who this helps: Patients and doctors managing insulin resistance and diabetes.

PubMed

Rosiglitazone reduces glucose-stimulated insulin secretion rate and increases insulin clearance in nondiabetic, insulin-resistant individuals.

2005

Diabetes

Kim SH, Abbasi F, Chu JW, McLaughlin TL, Lamendola C +2 more

Plain English
This study looked at how a medication called rosiglitazone affects insulin production and clearance in people who are not diabetic but are resistant to insulin. After 12 weeks of treatment, participants showed better insulin sensitivity, with their average blood glucose levels dropping significantly from 13.5 to 9.8 mmol/l. As a result, their insulin response decreased by 21%, and the rate at which their body cleared insulin increased by up to 34%. Who this helps: This benefits patients who are insulin-resistant, particularly those at risk for diabetes.

PubMed

Diabetic pancreatic beta cells ARNT all they should be.

2005

Cell metabolism

Levisetti MG, Polonsky KS

Plain English
Researchers studied the role of a protein called ARNT in the function of insulin-producing cells in the pancreas. They found that ARNT is less active in diabetic humans and that mice without ARNT developed problems like high blood sugar and poor insulin release, similar to type 2 diabetes. This matters because understanding how ARNT functions could lead to new treatments for diabetes. Who this helps: This helps patients with diabetes and their doctors.

PubMed

Two-hour seven-sample oral glucose tolerance test and meal protocol: minimal model assessment of beta-cell responsivity and insulin sensitivity in nondiabetic individuals.

2005

Diabetes

Dalla Man C, Campioni M, Polonsky KS, Basu R, Rizza RA +2 more

Plain English
This research looked into a simpler way to test how well insulin works in people without diabetes. By comparing a detailed test with a shorter one, researchers found that the reduced two-hour test still gave very similar results in measuring insulin response and sensitivity. Specifically, the shorter test produced results close to the longer test, showing that it can effectively assess insulin function with numbers very close to each other, indicating high reliability. Who this helps: This helps researchers and healthcare providers studying insulin function in nondiabetic individuals.

PubMed

Frequent Co-Authors

Bruce W Patterson Graeme I Bell Burton M Wice James D Johnson Eric L Ford Dan S Luciani Samuel Klein Hung Tran Dennis T Villareal Heather Robertson

Physician data sourced from the NPPES NPI Registry . Publication data from PubMed . Plain-English summaries generated by AI. Not medical advice.