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The purpose of this research study is to 1) understand how some, but not all people with obesity develop obesity related conditions such as type 2 diabetes and cardiovascular disease, and 2) compare the effects of 3 popular weight loss diets (Mediterranean, low-carbohydrate, or a very-low-fat plant-based diet) in people with obesity.
Obesity is associated with a constellation of cardiometabolic abnormalities (including insulin resistance, elevated blood pressure and dyslipidemia) that are risk factors for diabetes and cardiovascular disease. However, not all people experience the typical "complications" associated with obesity. Approximately 25% of obese people are protected from the adverse metabolic effects of excess fat accumulation and are considered metabolically-normal, based on their normal response to insulin. The mechanisms responsible for the development of insulin resistance and cardiometabolic complications in some, but not all, obese persons are unknown.
In people that do develop the typical "complications" associated with obesity weight loss has profound therapeutic effects. Currently, there are three distinctly different types of diets that have demonstrated considerable benefits in improving cardiometabolic health in both lean and obese people: 1) a Mediterranean diet, 2) a low-carbohydrate, ketogenic diet, and 3) a plant-based, very-low-fat diet. However, there is considerable inter-individual variability in body weight loss among people in response to any given diet, and it is not known why some people lose more weight with one diet than another. The mechanisms responsible for the different weight and metabolic responses to specific types of diets and the independent effects of weight loss and dietary macronutrient composition on cardiometabolic health are unclear.
The overarching goal of this project is therefore to fill these gaps in knowledge by conducting a careful cross-sectional characterization of metabolically normal lean, metabolically normal obese and metabolically abnormal obese individuals to compare body composition, body fat distribution, the plasma metabolome, systemic and adipose tissue inflammation and immune system function, adipose tissue and muscle biological function, the gut microbiome, the brain's structure, cognitive function and central reward mechanisms, and taste sensation between groups. . Metabolically abnormal obese participants will then be randomized to follow a Mediterranean, a low-carbohydrate ketogenic or a plant-based, very-low-fat diet to examine the different effects of these diets on the above outcomes with the purpose to determine the beneficial or potentially harmful effects of these different diets.
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| Label | Type | Description | Intervention Names |
|---|---|---|---|
| Metabolically normal lean - Baseline testing only | No Intervention | Metabolically normal lean - Lean individuals that have good glucose (sugar) control, normal plasma triglyceride (fat) levels and a low liver fat content. Dietary intervention - None. | |
| Metabolically normal obese - Baseline testing only | No Intervention | Metabolically normal obese - Persons with obesity that have good glucose (sugar) control, normal plasma triglyceride (fat) levels and a low liver fat content. Dietary intervention - None. | |
| Metabolically abnormal obese - Mediterranean diet | Experimental | Metabolically abnormal obese - Persons with obesity with glucose levels higher than recommended and a moderate to high amount of fat in the liver. Dietary intervention - A nutritionally balanced diet that includes fruits, vegetables, fish, beans, whole grains, and olive oil with approximately 50% of daily calories coming from complex carbohydrates, 30% of calories from fat, and 20% of calories from protein. |
|
| Metabolically abnormal obese - Low carbohydrate ketogenic diet | Experimental | Metabolically abnormal obese - Persons with obesity with glucose levels higher than recommended and a moderate to high amount of fat in the liver. Dietary intervention - A very-low-carbohydrate, adequate protein, high-fat diet containing 20 grams of carbohydrate or less per day (about 5% of calories), derived mainly from vegetables. |
| Name | Type | Description | Arm Group Labels | Other Names |
|---|---|---|---|---|
| Metabolically abnormal obese - Mediterranean diet | Other | The effect of consuming a Mediterranean diet will be examined over 3 different phases: (i) weight maintenance for 4 to 8 weeks, with all meals provided; (ii) controlled 7-10% weight loss with caloric intake reduced by 25% to achieve the desired amount of weight loss in about 4 to 5 months with all meals provided; and (iii) Independent weight loss for about 4 months. During the independent weight loss phase of the study subjects will be asked to continue to consume a Mediterranean diet but will prepare all their food at home. No food will be provided during this portion of the study. |
| Measure | Description | Time Frame |
|---|---|---|
| Insulin sensitivity | Whole-body insulin sensitivity will be assessed by using the hyperinsulinemic-euglycemic clamp procedure | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in insulin sensitivity | Whole-body insulin sensitivity will be assessed by using the hyperinsulinemic-euglycemic clamp procedure | Before and after 4 to 8-weeks of weight maintenance and after 7-10% weight loss (~6-7 months) |
| Measure | Description | Time Frame |
|---|---|---|
| 24-hour glucose concentrations | Glucose concentrations will be evaluated from frequent blood samples over a 24 h period | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in 24-hour glucose concentrations |
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Inclusion Criteria:
Exclusion Criteria:
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| Name | Affiliation | Role |
|---|---|---|
| Samuel Klein, MD | Washington University School of Medicine | Principal Investigator |
| Facility | Status | City | State | ZIP | Country | Contacts |
|---|---|---|---|---|---|---|
| Washington University School of Medicine | St Louis | Missouri | 63110 | United States |
| PubMed Identifier | Type | Citation | Retractions |
|---|---|---|---|
| 38569471 | Background | Petersen MC, Smith GI, Palacios HH, Farabi SS, Yoshino M, Yoshino J, Cho K, Davila-Roman VG, Shankaran M, Barve RA, Yu J, Stern JH, Patterson BW, Hellerstein MK, Shulman GI, Patti GJ, Klein S. Cardiometabolic characteristics of people with metabolically healthy and unhealthy obesity. Cell Metab. 2024 Apr 2;36(4):745-761.e5. doi: 10.1016/j.cmet.2024.03.002. | |
| 38228469 |
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| Metabolically abnormal obese - Plant-based very-low-fat diet | Experimental | Metabolically abnormal obese - Persons with obesity with glucose levels higher than recommended and a moderate to high amount of fat in the liver. Dietary intervention - A plant-based diet high in complex carbohydrates and low in fat, protein, and sodium, with approximately 70% of daily calories from carbohydrates, 15% from fat, and 15% from protein. |
|
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| Metabolically abnormal obese - Low carbohydrate ketogenic diet | Other | The effect of consuming a low-carbohydrate, ketogenic diet will be examined over 3 different phases: (i) weight maintenance for 4 to 8 weeks, with all meals provided; (ii) controlled 7-10% weight loss with caloric intake reduced by 25% to achieve the desired amount of weight loss in about 4 to 5 months with all meals provided; and (iii) Independent weight loss for about 4 months. During the independent weight loss phase of the study subjects will be asked to continue to consume a low carbohydrate ketogenic diet but will prepare all their food at home. No food will be provided during this portion of the study. |
|
| Metabolically abnormal obese - Plant-based, very-low-fat diet | Other | The effect of consuming a plant-based, very-low-fat diet will be examined over 3 different phases: (i) weight maintenance for 4 to 8 weeks, with all meals provided; (ii) controlled 7-10% weight loss with caloric intake reduced by 25% to achieve the desired amount of weight loss in about 4 to 5 months with all meals provided; and (iii) Independent weight loss for about 4 months. During the independent weight loss phase of the study subjects will be asked to continue to consume a plant-based, very-low-fat diet but will prepare all their food at home. No food will be provided during this portion of the study. |
|
| Annual Follow-up Visits | Behavioral | Metabolic health will be assessed 1 and 2-years after competing the diet intervention study. No intervention will be performed during the time. |
|
Glucose concentrations will be evaluated from frequent blood samples over a 24 h period |
| Before and after 4 to 8-weeks of weight maintenance and after 7-10% weight loss (~6-7 months) |
| 24-hour hormone concentrations | Plasma hormone concentrations will be evaluated from frequent blood sampling over a 24 h period | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in 24-hour hormone concentrations | Plasma hormone concentrations will be evaluated from frequent blood sampling over a 24 h period | Before and after 4 to 8-weeks of weight maintenance and after 7-10% weight loss (~6-7 months) |
| 24-hour cytokine concentrations | Plasma cytokine concentrations will be evaluated from frequent blood sampling over a 24 h period | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| β-cell function | β-cell function will be assessed from a modified oral glucose tolerance test | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in β-cell function | β-cell function will be assessed from a modified oral glucose tolerance test | Before and after 7-10% weight loss (~6-7 months) and independent weight loss (12 months) in metabolically abnormal obese individuals only. |
| Insulin clearance | Insulin clearance will be assessed from a modified oral glucose tolerance test and hyperinsulinemic-euglycemic clamp procedure | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Insulin clearance | Insulin clearance will be assessed from a modified oral glucose tolerance test and hyperinsulinemic-euglycemic clamp procedure | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only. |
| Fat mass and fat free mass | Fat mass and fat free mass will be assessed using dual-energy x-ray absorptiometry (DXA) | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in fat mass and fat free mass | Fat mass and fat free mass will be assessed using dual-energy x-ray absorptiometry (DXA) | Before and after 4 to 8-weeks of weight maintenance, after 7-10% weight loss (~6-7 months) and after independent weight loss (12 months) |
| Exosome-mediated intercellular signaling | Signaling between cells and organs will be examined by isolating exosomes (small extracellular vesicles) from blood and adipose tissue | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in exosome-mediated intercellular signaling | Signaling between cells and organs will be examined by isolating exosomes (small extracellular vesicles) from blood and adipose tissue | Before and after 4 to 8-weeks of weight maintenance, after 7-10% weight loss (~6-7 months) and after independent weight loss (12 months) |
| Abdominal adipose tissue volumes | Abdominal subcutaneous and intra-abdominal adipose tissue volumes will be assessed by magnetic resonance imagining (MRI) | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in abdominal adipose tissue volumes | Abdominal subcutaneous and intra-abdominal adipose tissue volumes will be assessed by magnetic resonance imagining (MRI) | Before and after 4 to 8-weeks of weight maintenance, after 7-10% weight loss (~6-7 months) and after independent weight loss (12 months) |
| Leg adipose tissue volumes | Thigh and calf adipose tissue volumes will be assessed by magnetic resonance imagining (MRI) | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in leg adipose tissue volumes | Thigh and calf adipose tissue volumes will be assessed by magnetic resonance imagining (MRI) | Before and after 4 to 8-weeks of weight maintenance, after 7-10% weight loss (~6-7 months) and after independent weight loss (12 months) |
| Intra-hepatic triglyceride content | Intra-hepatic triglyceride content will be assessed by magnetic resonance techniques | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in intra-hepatic triglyceride content | Intra-hepatic triglyceride content will be assessed by magnetic resonance techniques | Before and after 4 to 8-weeks of weight maintenance, after 7-10% weight loss (~6-7 months) and after independent weight loss (12 months) |
| Gut microbiome | Gut microbiota, meta-transcriptome (bacterial RNA sequencing to determine what proteins can be made by the microbiota) and the meta-metabolome (metabolites made by the microbiota) will be assessed | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in gut microbiome | Gut microbiota, meta-transcriptome (bacterial RNA sequencing to determine what proteins can be made by the microbiota) and the meta-metabolome (metabolites made by the microbiota) will be assessed | Before and during 4 to 8-weeks of weight maintenance, 7-10% weight loss (~6-7 months) and independent weight loss (12 months) |
| Plasma lipid profile | Fasting plasma lipid profile will be assessed by nuclear magnetic resonance (NMR) techniques | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in plasma lipid profile | Fasting plasma lipid profile will be assessed by nuclear magnetic resonance (NMR) techniques | Before and after 4 to 8-weeks of weight maintenance, after 7-10% weight loss (~6-7 months) and after independent weight loss (12 months) |
| Aerobic fitness | Maximal oxygen consumption will be assessed using indirect calorimetry during a graded exercise test to volitional fatigue | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in aerobic fitness | Maximal oxygen consumption will be assessed using indirect calorimetry during a graded exercise test to volitional fatigue | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals randomized to the plant-based very-low-fat diet only |
| Carotid artery intima media thickness | Carotid artery intima media thickness will be assessed by ultrasound imaging | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in carotid artery intima media thickness | Carotid artery intima media thickness will be assessed by ultrasound imaging | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only |
| Cardiac structure and function | Ultrasound techniques will be used to assess cardiac structure and function | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in cardiac structure and function | Ultrasound techniques will be used to assess cardiac structure and function | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only |
| Endothelial function | Endothelial function will be assessed using a non-invasive device (EndoPat 2000) in response to reactive hyperemia. | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in endothelial function | Endothelial function will be assessed using a non-invasive device (EndoPat 2000) in response to reactive hyperemia. | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only |
| Arterial stiffness | Arterial stiffness will be assessed using a non-invasive device (SphygmoCor) | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in arterial stiffness | Arterial stiffness will be assessed using a non-invasive device (SphygmoCor) | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only |
| Physical activity | Physical activity will be assessed using tri-axial accelerometry | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in physical activity | Physical activity will be assessed using tri-axial accelerometry | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only |
| Sleep efficiency | Sleep efficiency will be assessed using tri-axial accelerometry | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in sleep efficiency | Sleep efficiency will be assessed using tri-axial accelerometry | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only |
| Rate of incorporation of 2H2O into lipids | Metabolic pathways relating to lipid (fat) synthesis in the liver and adipose tissue (fat) will be assessed by heavy water (2H2O) ingestion followed by fat biopsies and blood sampling | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in the rate of incorporation of 2H2O into lipids | Metabolic pathways relating to lipid (fat) synthesis in the liver and adipose tissue (fat) will be assessed by heavy water (2H2O) ingestion followed by fat biopsies and blood sampling | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only |
| Rate of incorporation of 2H2O into proteins | Metabolic pathways relating to protein synthesis in the muscle and adipose tissue will be assessed by heavy water (2H2O) ingestion followed by skeletal muscle and and adipose tissue biopsies and blood sampling | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in the rate of incorporation of 2H2O into proteins | Metabolic pathways relating to protein synthesis in the muscle and adipose tissue will be assessed by heavy water (2H2O) ingestion followed by skeletal muscle and and adipose tissue biopsies and blood sampling | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only |
| Taste intensity | Subjects will be evaluated by using the NIH toolbox Taste Intensity Test | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in taste intensity | Subjects will be evaluated by using the NIH toolbox Taste Intensity Test | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only |
| Sweet taste palatability | Sweet palatability will be assessed using the general Labeled Magnitude Scale | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in sweet taste palatability | Sweet palatability will be assessed using the general Labeled Magnitude Scale | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only |
| Immune function | Immune cell populations within plasma and adipose tissue will be profiled using multi-color fluorescence activated cell sorting (FACS) techniques. | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in immune function | Immune cell populations within plasma and adipose tissue will be profiled using multi-color fluorescence activated cell sorting (FACS) techniques. | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only |
| Food consumption-induced changes in brain blood flow | Food consumption-induced changes in brain blood flow will be assessed by blood-oxygen dependent (BOLD) and arterial spin labeling using functional magnetic resonance imaging (fMRI) techniques | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in food consumption-induced changes in brain blood flow | Food consumption-induced changes in brain blood flow will be assessed by blood-oxygen dependent (BOLD) and arterial spin labeling using functional magnetic resonance imaging (fMRI) techniques | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only |
| Transcriptome in blood, muscle and adipose tissue | The transcriptome (all RNA that are responsible for making proteins from DNA templates) will be evaluated by using RNA sequencing techniques | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in transcriptome in blood, muscle and adipose tissue | The transcriptome (all RNA that are responsible for making proteins from DNA templates) will be evaluated by using RNA sequencing techniques | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only |
| Epigenome in blood, muscle and adipose tissue | The epigenome (chemical modifications of DNA that signal genes to be on or off) will be evaluated by using Illumina Infinium HumanMethylation450 BeadChip assays. | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in epigenome in blood, muscle and adipose tissue | The epigenome (chemical modifications of DNA that signal genes to be on or off) will be evaluated by using Illumina Infinium HumanMethylation450 BeadChip assays. | Before and after 7-10% weight loss (~6-7 months) in metabolically abnormal obese individuals only |
| Dopamine receptor binding potential | Dopamine receptor binding potential will be assessed by Positron Emission Tomography (PET) using [11C]raclopride in the fasted and fed states | Baseline in fasted and fed states in metabolically abnormal obese participants only. |
| Subcutaneous abdominal adipose tissue oxygen tension | Oxygen tension will be assessed in subcutaneous abdominal adipose tissue in the abdomen using oxygen-sensitive fiber-optic probes (OxyLiteTM, Oxford Optronix, Ltd) | Baseline only (cross-sectional comparison of metabolically normal lean, metabolically normal obese and metabolically abnormal obese subjects). |
| Change in β-cell function | β-cell function will be assessed from a modified oral glucose tolerance test | Before and at annual follow-up visits (assessed up to 2 years) in metabolically abnormal obese individuals only. |
| Insulin clearance | Insulin clearance will be assessed from a modified oral glucose tolerance test | Before and at annual follow-up visits (assessed up to 2 years) in metabolically abnormal obese individuals only. |
| Change in fat mass and fat free mass | Fat mass and fat free mass will be assessed using dual-energy x-ray absorptiometry (DXA) | Before and at annual follow-up visits (assessed up to 2 years) in metabolically abnormal obese individuals only. |
| Change in intra-hepatic triglyceride content | Intra-hepatic triglyceride content will be assessed by magnetic resonance techniques | Before and at annual follow-up visits (assessed up to 2 years) in metabolically abnormal obese individuals only. |
| Mittendorfer B, van Vliet S, Smith GI, Petersen MC, Patterson BW, Klein S. Impaired plasma glucose clearance is a key determinant of fasting hyperglycemia in people with obesity. Obesity (Silver Spring). 2024 Mar;32(3):540-546. doi: 10.1002/oby.23963. Epub 2024 Jan 16. |
| 31528845 | Result | Seo JB, Riopel M, Cabrales P, Huh JY, Bandyopadhyay GK, Andreyev AY, Murphy AN, Beeman SC, Smith GI, Klein S, Lee YS, Olefsky JM. Knockdown of Ant2 Reduces Adipocyte Hypoxia And Improves Insulin Resistance in Obesity. Nat Metab. 2019 Jan;1(1):86-97. doi: 10.1038/s42255-018-0003-x. Epub 2018 Nov 19. |
| 31454790 | Result | Stern JH, Smith GI, Chen S, Unger RH, Klein S, Scherer PE. Obesity dysregulates fasting-induced changes in glucagon secretion. J Endocrinol. 2019 Nov;243(2):149-160. doi: 10.1530/JOE-19-0201. |
| 32086877 | Result | Eisenstein SA, Black KJ, Samara A, Koller JM, Dunn JP, Hershey T, Klein S, Smith GI. Striatal Dopamine Responses to Feeding are Altered in People with Obesity. Obesity (Silver Spring). 2020 Apr;28(4):765-771. doi: 10.1002/oby.22753. Epub 2020 Feb 21. |
| 32099031 | Result | Ding X, Iyer R, Novotny C, Metzger D, Zhou HH, Smith GI, Yoshino M, Yoshino J, Klein S, Swaminath G, Talukdar S, Zhou Y. Inhibition of Grb14, a negative modulator of insulin signaling, improves glucose homeostasis without causing cardiac dysfunction. Sci Rep. 2020 Feb 25;10(1):3417. doi: 10.1038/s41598-020-60290-1. |
| 32191646 | Result | Smith GI, Polidori DC, Yoshino M, Kearney ML, Patterson BW, Mittendorfer B, Klein S. Influence of adiposity, insulin resistance, and intrahepatic triglyceride content on insulin kinetics. J Clin Invest. 2020 Jun 1;130(6):3305-3314. doi: 10.1172/JCI136756. |
| 31805015 | Result | Smith GI, Shankaran M, Yoshino M, Schweitzer GG, Chondronikola M, Beals JW, Okunade AL, Patterson BW, Nyangau E, Field T, Sirlin CB, Talukdar S, Hellerstein MK, Klein S. Insulin resistance drives hepatic de novo lipogenesis in nonalcoholic fatty liver disease. J Clin Invest. 2020 Mar 2;130(3):1453-1460. doi: 10.1172/JCI134165. |
| 33164985 | Result | Cifarelli V, Beeman SC, Smith GI, Yoshino J, Morozov D, Beals JW, Kayser BD, Watrous JD, Jain M, Patterson BW, Klein S. Decreased adipose tissue oxygenation associates with insulin resistance in individuals with obesity. J Clin Invest. 2020 Dec 1;130(12):6688-6699. doi: 10.1172/JCI141828. |
| 33743554 | Result | Beals JW, Smith GI, Shankaran M, Fuchs A, Schweitzer GG, Yoshino J, Field T, Matthews M, Nyangau E, Morozov D, Mittendorfer B, Hellerstein MK, Klein S. Increased Adipose Tissue Fibrogenesis, Not Impaired Expandability, Is Associated With Nonalcoholic Fatty Liver Disease. Hepatology. 2021 Sep;74(3):1287-1299. doi: 10.1002/hep.31822. Epub 2021 Jun 22. |
| 34004161 | Result | Fuchs A, Samovski D, Smith GI, Cifarelli V, Farabi SS, Yoshino J, Pietka T, Chang SW, Ghosh S, Myckatyn TM, Klein S. Associations Among Adipose Tissue Immunology, Inflammation, Exosomes and Insulin Sensitivity in People With Obesity and Nonalcoholic Fatty Liver Disease. Gastroenterology. 2021 Sep;161(3):968-981.e12. doi: 10.1053/j.gastro.2021.05.008. Epub 2021 May 15. |
| 35817849 | Result | Farabi SS, Smith GI, Schweitzer GG, Stein RI, Klein S. Do lifestyle factors and quality of life differ in people with metabolically healthy and unhealthy obesity? Int J Obes (Lond). 2022 Oct;46(10):1778-1785. doi: 10.1038/s41366-022-01180-6. Epub 2022 Jul 11. |
| 34905513 | Result | Mittendorfer B, Patterson BW, Smith GI, Yoshino M, Klein S. beta Cell function and plasma insulin clearance in people with obesity and different glycemic status. J Clin Invest. 2022 Feb 1;132(3):e154068. doi: 10.1172/JCI154068. |
| 37475685 | Result | Dunn JP, Lamichhane B, Smith GI, Garner A, Wallendorf M, Hershey T, Klein S. Dorsal striatal response to taste is modified by obesity and insulin resistance. Obesity (Silver Spring). 2023 Aug;31(8):2065-2075. doi: 10.1002/oby.23799. |
| 37365374 | Result | Beals JW, Kayser BD, Smith GI, Schweitzer GG, Kirbach K, Kearney ML, Yoshino J, Rahman G, Knight R, Patterson BW, Klein S. Dietary weight loss-induced improvements in metabolic function are enhanced by exercise in people with obesity and prediabetes. Nat Metab. 2023 Jul;5(7):1221-1235. doi: 10.1038/s42255-023-00829-4. Epub 2023 Jun 26. |
| ID | Term |
|---|---|
| D009765 | Obesity |
| D007333 | Insulin Resistance |
| ID | Term |
|---|---|
| D050177 | Overweight |
| D044343 | Overnutrition |
| D009748 | Nutrition Disorders |
| D009750 | Nutritional and Metabolic Diseases |
| D001835 | Body Weight |
| D012816 | Signs and Symptoms |
| D013568 | Pathological Conditions, Signs and Symptoms |
| D006946 | Hyperinsulinism |
| D044882 | Glucose Metabolism Disorders |
| D008659 | Metabolic Diseases |
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