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1. Metabolic response to high-carbohydrate and low-carbohydrate meals in a nonhuman primate model.

Author

Fabbrini E, Higgins PB, Magkos F, Bastarrachea RA, Voruganti VS, Comuzzie AG, Shade RE, Gastaldelli A, Horton JD, Omodei D, Patterson BW, and Klein S

Subjects
Animals, Blood Glucose analysis, C-Reactive Protein analysis, Carbon Radioisotopes, Cross-Over Studies, Deuterium, Diet, Carbohydrate-Restricted adverse effects, Diet, High-Fat adverse effects, Dietary Carbohydrates adverse effects, Dietary Carbohydrates metabolism, Glucagon blood, Glucagon metabolism, Gluconeogenesis, Insulin blood, Insulin Secretion, Male, Models, Biological, Papio hamadryas, Postprandial Period, Random Allocation, Dietary Carbohydrates administration & dosage, Glucose metabolism, Insulin metabolism, Islets of Langerhans metabolism, Meals
Abstract

We established a model of chronic portal vein catheterization in an awake nonhuman primate to provide a comprehensive evaluation of the metabolic response to low-carbohydrate/high-fat (LCHF; 20% carbohydrate and 65% fat) and high-carbohydrate/low-fat (HCLF; 65% carbohydrate and 20% fat) meal ingestion. Each meal was given 1 wk apart to five young adult (7.8 ± 1.3 yr old) male baboons. A [U-¹³C]glucose tracer was added to the meal, and a [6,6-²H₂]glucose tracer was infused systemically to assess glucose kinetics. Plasma areas under the curve (AUCs) of glucose, insulin, and C-peptide in the femoral artery and of glucose and insulin in the portal vein were higher (P ≤ 0.05) after ingestion of the HCLF compared with the LCHF meal. Compared with the LCHF meal, the rate of appearance of ingested glucose into the portal vein and the systemic circulation was greater after the HCLF meal (P < 0.05). Endogenous glucose production decreased by ∼40% after ingestion of the HCLF meal but was not affected by the LCHF meal (P < 0.05). Portal vein blood flow increased (P < 0.001) to a similar extent after consumption of either meal. In conclusion, a LCHF diet causes minimal changes in the rate of glucose appearance in both portal and systemic circulations, does not affect the rate of endogenous glucose production, and causes minimal stimulation of C-peptide and insulin. These observations demonstrate that LCHF diets cause minimal perturbations in glucose homeostasis and pancreatic β-cell activity.

Published
2013
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2. Portal vein and systemic adiponectin concentrations are closely linked with hepatic glucose and lipoprotein kinetics in extremely obese subjects.

Author

Magkos F, Fabbrini E, Patterson BW, Eagon JC, and Klein S

Subjects
Adiponectin analysis, Adiponectin blood, Adiponectin metabolism, Adult, Female, Humans, Kinetics, Lipoproteins, VLDL blood, Male, Middle Aged, Obesity, Morbid blood, Osmolar Concentration, Radioactive Tracers, Glucose metabolism, Lipoproteins, VLDL metabolism, Liver metabolism, Obesity, Morbid metabolism, Portal Vein metabolism
Abstract

Low systemic plasma adiponectin concentrations are associated with abnormalities in hepatic glucose and lipoprotein metabolism in obese people. However, the relationship between the delivery of adiponectin to the liver via the portal vein and hepatic glucose and lipoprotein metabolism is not known. We examined the relationship between hepatic substrate metabolism (glucose rate of appearance into plasma and hepatic very low-density lipoprotein [VLDL]-triglyceride [TG] and VLDL-apolipoprotein B-100 [apoB-100] secretion rates, determined by using stable isotope-labeled tracer techniques) and portal vein adiponectin concentration, in 8 insulin-resistant, extremely obese subjects (body mass index, 65 ± 7 kg/m(2)). Portal vein adiponectin concentration was inversely associated with basal glucose rate of appearance (r = -0.820, P = .013) and VLDL-TG (r = -0.823, P = .012) and VLDL-apoB-100 (r = -0.787, P = .020) secretion rates. Very similar correlations were obtained for radial artery adiponectin as a result of a mirroring relationship between portal and arterial adiponectin concentrations (r = 0.899, P = .002) and the absence of significant arteriovenous concentration differences (P = .570). Insulin resistance, assessed with the homeostasis model assessment score, was also strongly associated with hepatic glucose and lipid metabolic parameters, as well as with adiponectin concentrations in the portal vein and radial artery. These results suggest that adiponectin delivery to the liver, whether via the portal or the systemic circulation, may be an important regulator of basal hepatic glucose, VLDL-TG, and VLDL-apoB-100 production rates in obese people, possibly through direct effects on the liver or changes in hepatic insulin sensitivity. However, portal vein adiponectin does not appear to be superior to arterial adiponectin as a marker of hepatic metabolic dysregulation. Additional studies are needed to elucidate the mechanism(s) responsible for the strong association we observed between adiponectin and hepatic substrate metabolism., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Published
2011
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3. Reproducibility of glucose, fatty acid and VLDL kinetics and multi-organ insulin sensitivity in obese subjects with non-alcoholic fatty liver disease.

Author

Magkos F, Fabbrini E, Korenblat K, Okunade AL, Patterson BW, and Klein S

Subjects
Adult, Fatty Liver epidemiology, Female, Humans, Male, Muscle, Skeletal metabolism, Non-alcoholic Fatty Liver Disease, Obesity epidemiology, Reproducibility of Results, Triglycerides metabolism, Adipose Tissue metabolism, Fatty Acids, Nonesterified metabolism, Fatty Liver metabolism, Glucose metabolism, Insulin Resistance, Lipoproteins, VLDL metabolism, Obesity metabolism
Abstract

Objective: Non-alcoholic fatty liver disease (NAFLD) is associated with abnormalities in basal glucose and free fatty acid (FFA) metabolism, multi-organ insulin resistance and alterations in lipoprotein kinetics. These metabolic outcomes can be evaluated in vivo by using stable isotopically labeled tracer methods. An understanding of the reproducibility of these measures is necessary to ensure adequate statistical power in studies designed to evaluate metabolic function in subjects with NAFLD., Methods: We determined the degree of intra-individual variability of skeletal muscle, adipose tissue, and hepatic insulin sensitivity and basal plasma glucose, FFA, and very-low-density lipoprotein triglyceride and apolipoprotein B-100 (apoB-100) kinetics in eight obese subjects with NAFLD (age: 44 ± 3 years; body mass index: 38.2 ± 1.7 kg m(-2); intrahepatic triglyceride content: 24.5 ± 3.9%), by using the hyperinsulinemic-euglycemic clamp technique and stable isotope-labeled tracer methods and mathematical modeling on two separate occasions ∼2 months apart., Results: The intra-individual variability (coefficient of variation) ranged from 6% for basal glucose production to 21% for insulin-stimulated glucose disposal (percentage increase from basal). We estimated that a 25% difference in any outcome measure can be detected with a sample size of ≤ 8 subjects for paired studies and ≤ 15 subjects per group for unpaired studies, assuming an α value of 0.05 and a β value of 0.20 (that is, 80% power)., Conclusion: These results demonstrate that only a small number of subjects are needed to detect clinically relevant effects in insulin sensitivity and hepatic lipoprotein metabolism in obese subjects with NAFLD, and will be useful to determine appropriate sample size for future metabolic studies.

Published
2011
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4. Multiorgan Insulin Sensitivity in Lean and Obese Subjects

Author

Bettina Mittendorfer, Elisa Fabbrini, Bruce W. Patterson, Samuel Klein, Caterina Conte, Marleen Kars, Interne Geneeskunde, RS: NUTRIM - R1 - Metabolic Syndrome, Conte, C, Fabbrini, E, Kars, M, Mittendorfer, B, Patterson, B, and Klein, S

Subjects
Blood Glucose, Male, Endocrinology, Diabetes and Metabolism, Glucose uptake, medicine.medical_treatment, Adipose tissue, FATTY-ACID-METABOLISM, Body Mass Index, GLUCOSE, 0302 clinical medicine, Non-alcoholic Fatty Liver Disease, Hyperinsulinemia, Insulin, Medicine, IN-VIVO, Original Research, 0303 health sciences, HUMANS, Skeletal, Middle Aged, MUSCLE, Glucose clamp technique, Adipose Tissue, Liver, CARDIOVASCULAR-DISEASE, Sedentary Lifestyle, Muscle, Female, Human, Adult, medicine.medical_specialty, Lipolysis, LIPOPROTEIN-LIPASE, 030209 endocrinology & metabolism, 03 medical and health sciences, Insulin resistance, Diabetes mellitus, Internal medicine, Internal Medicine, Obesity, Pathophysiology/Complications, Muscle, Skeletal, Triglycerides, Dyslipidemias, 030304 developmental biology, Advanced and Specialized Nursing, business.industry, Settore MED/13 - ENDOCRINOLOGIA, DIABETES-MELLITUS, medicine.disease, Lipolysi, Fatty Liver, Endocrinology, Dyslipidemia, Glucose Clamp Technique, HUMAN ADIPOSE, Insulin Resistance, Sedentary Behavior, business, RESISTANCE
Abstract

OBJECTIVE To provide a comprehensive assessment of multiorgan insulin sensitivity in lean and obese subjects with normal glucose tolerance. RESEARCH DESIGN AND METHODS The hyperinsulinemic-euglycemic clamp procedure with stable isotopically labeled tracer infusions was performed in 40 obese (BMI 36.2 ± 0.6 kg/m2, mean ± SEM) and 26 lean (22.5 ± 0.3 kg/m2) subjects with normal glucose tolerance. Insulin was infused at different rates to achieve low, medium, and high physiological plasma concentrations. RESULTS In obese subjects, palmitate and glucose Ra in plasma decreased with increasing plasma insulin concentrations. The decrease in endogenous glucose Ra was greater during low-, medium-, and high-dose insulin infusions (69 ± 2, 74 ± 2, and 90 ± 2%) than the suppression of palmitate Ra (52 ± 4, 68 ± 1, and 79 ± 1%). Insulin-mediated increase in glucose disposal ranged from 24 ± 5% at low to 253 ± 19% at high physiological insulin concentrations. The suppression of palmitate Ra and glucose Ra were greater in lean than obese subjects during low-dose insulin infusion but were the same in both groups during high-dose insulin infusion, whereas stimulation of glucose Rd was greater in lean than obese subjects across the entire physiological range of plasma insulin. CONCLUSIONS Endogenous glucose production and adipose tissue lipolytic rate are both very sensitive to small increases in circulating insulin, whereas stimulation of muscle glucose uptake is minimal until high physiological plasma insulin concentrations are reached. Hyperinsulinemia within the normal physiological range can compensate for both liver and adipose tissue insulin resistance, but not skeletal muscle insulin resistance, in obese people who have normal glucose tolerance.

Published
2012
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5. Adipose and muscle tissue profile of CD36 transcripts in obese subjects highlights the role of CD36 in fatty acid homeostasis and insulin resistance

Author

Samuel Klein, Bruce W. Patterson, Caterina Conte, Timothy Schappe, Latisha Love-Gregory, Nada A. Abumrad, Terri A. Pietka, Elisa Fabbrini, Pietka, T, Schappe, T, Conte, C, Fabbrini, E, Patterson, B, Klein, S, Abumrad, N, and Love-Gregory, L

Subjects
Adult, CD36 Antigens, Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Adipose tissue, 030209 endocrinology & metabolism, Carbohydrate metabolism, cd36, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Insulin resistance, Internal medicine, Adipocyte, parasitic diseases, Internal Medicine, Adipocytes, Medicine, Homeostasis, Humans, Obesity, Fatty acid homeostasis, Muscle, Skeletal, Pathophysiology/Complications, Triglycerides, 030304 developmental biology, Advanced and Specialized Nursing, 0303 health sciences, business.industry, Fatty Acids, Skeletal muscle, Settore MED/13 - ENDOCRINOLOGIA, hemic and immune systems, Glucose clamp technique, medicine.disease, adipose tissue, medicine.anatomical_structure, Endocrinology, Glucose, chemistry, Adipose Tissue, Liver, Glucose Clamp Technique, Female, Metabolic syndrome, Insulin Resistance, business
Abstract

OBJECTIVE Fatty acid (FA) metabolism is tightly regulated across several tissues and impacts insulin sensitivity. CD36 facilitates cellular FA uptake, and CD36 genetic variants associate with lipid abnormalities and susceptibility to metabolic syndrome. The objective of this study was to gain insight regarding the in vivo metabolic influence of muscle and adipose tissue CD36. For this, we determined the relationships between CD36 alternative transcripts, which can reflect tissue-specific CD36 regulation, and measures of FA metabolism and insulin resistance. RESEARCH DESIGN AND METHODS The relative abundance of alternative CD36 transcripts in adipose tissue and skeletal muscle from 53 nondiabetic obese subjects was measured and related to insulin sensitivity and FA metabolism assessed by hyperinsulinemic–euglycemic clamps and isotopic tracers for glucose and FA. RESULTS Transcript 1C, one of two major transcripts in adipose tissue, that is restricted to adipocytes predicted systemic and tissue (adipose, liver, and muscle) insulin sensitivity, suggesting adipocyte CD36 protects against insulin resistance. Transcripts 1B and 1A, the major transcripts in skeletal muscle, correlated with FA disposal rate and triglyceride clearance, supporting importance of muscle CD36 in clearance of circulating FA. Additionally, the common CD36 single nucleotide polymorphism rs1761667 selectively influenced CD36 transcripts and exacerbated insulin resistance of glucose disposal by muscle. CONCLUSIONS Alternative CD36 transcripts differentially influence tissue CD36 and consequently FA homeostasis and insulin sensitivity. Adipocyte CD36 appears to be metabolically protective, and its selective upregulation might have therapeutic potential in insulin resistance.

Published
2014

6. Association between specific adipose tissue CD4+ T-cell populations and insulin resistance in obese individuals

Author

Elisa Fabbrini, Faidon Magkos, David Bradley, Zhouji Chen, J. Christopher Eagon, Steve A. Mccartney, Marina Cella, Caterina Conte, Samuel Klein, Dong Ho Han, Bruce W. Patterson, Gemma Fraterrigo, Nada A. Abumrad, Terri A. Pietka, Anja Fuchs, Brian N. Finck, Marco Colonna, Fabbrini, E, Cella, M, Mccartney, Sa, Fuchs, A, Abumrad, Na, Pietka, Ta, Chen, Z, Finck, Bn, Han, Dh, Magkos, F, Conte, Caterina, Bradley, D, Fraterrigo, G, Eagon, Jc, Patterson, Bw, Colonna, M, and Klein, S.

Subjects
CD4-Positive T-Lymphocytes, FFM, nonalcoholic fatty liver disease, Male, medicine.medical_treatment, Adipose tissue, White adipose tissue, Body Mass Index, T-Lymphocyte Subsets, Receptors, Nonalcoholic fatty liver disease, Hepatocyte, Lymphocytes, GIF, Receptors, Interleukin-17, interleukin, Interleukin-17, Gastroenterology, interferon, Skeletal, Glucose clamp technique, Middle Aged, Cytokine, medicine.anatomical_structure, Liver, metabolically normal insulin-sensitive obese, CD4-Positive T-Lymphocyte, MAO, Cytokines, metabolically abnormal insulin-resistant obese, Muscle, Lymphocyte, Female, Case-Control Studie, Human, Receptor, Adult, medicine.medical_specialty, MNO, Adipose tissue macrophages, Subcutaneous Fat, glucose infusion rate, T-Lymphocyte Subset, Biology, fat free ma, IFN, Article, Insulin resistance, Internal medicine, NAFLD, medicine, Animals, Humans, Obesity, Muscle, Skeletal, Hepatology, Metabolically Abnormal Obesity, Animal, Interleukin-6, Interleukins, c-Jun kinase, Skeletal muscle, Settore MED/13 - ENDOCRINOLOGIA, IL, Receptors, Interleukin, medicine.disease, Rats, Endocrinology, Glucose, Case-Control Studies, Hepatocytes, Glucose Clamp Technique, fat free mass, Rat, Th17 Cells, JNK, Insulin Resistance, Metabolically Normal Obesity
Abstract

Background & Aims An increased number of macrophages in adipose tissue is associated with insulin resistance and metabolic dysfunction in obese people. However, little is known about other immune cells in adipose tissue from obese people, and whether they contribute to insulin resistance. We investigated the characteristics of T cells in adipose tissue from metabolically abnormal insulin-resistant obese (MAO) subjects, metabolically normal insulin-sensitive obese (MNO) subjects, and lean subjects. Insulin sensitivity was determined by using the hyperinsulinemic euglycemic clamp procedure. Methods We assessed plasma cytokine concentrations and subcutaneous adipose tissue CD4 + T-cell populations in 9 lean, 12 MNO, and 13 MAO subjects. Skeletal muscle and liver samples were collected from 19 additional obese patients undergoing bariatric surgery to determine the presence of selected cytokine receptors. Results Adipose tissue from MAO subjects had 3- to 10-fold increases in numbers of CD4 + T cells that produce interleukin (IL)-22 and IL-17 (a T-helper [Th] 17 and Th22 phenotype) compared with MNO and lean subjects. MAO subjects also had increased plasma concentrations of IL-22 and IL-6. Receptors for IL-17 and IL-22 were expressed in human liver and skeletal muscle samples. IL-17 and IL-22 inhibited uptake of glucose in skeletal muscle isolated from rats and reduced insulin sensitivity in cultured human hepatocytes. Conclusions Adipose tissue from MAO individuals contains increased numbers of Th17 and Th22 cells, which produce cytokines that cause metabolic dysfunction in liver and muscle in vitro. Additional studies are needed to determine whether these alterations in adipose tissue T cells contribute to the pathogenesis of insulin resistance in obese people.

Published
2013

7. Intrahepatic diacylglycerol content is associated with hepatic insulin resistance in obese subjects

Author

J. Christopher Eagon, Bruce W. Patterson, Elizabeth M. Brunt, Faidon Magkos, Xiong Su, Caterina Conte, David Bradley, Samuel Klein, J. Esteban Varela, Elisa Fabbrini, Magkos, F, Su, X, Bradley, D, Fabbrini, E, Conte, C, Eagon, J, Varela, J, Brunt, E, Patterson, B, and Klein, S

Subjects
Adult, Male, medicine.medical_specialty, Ceramide, Diglyceride, medicine.medical_treatment, Carbohydrate metabolism, Biology, Ceramides, Article, Diglycerides, chemistry.chemical_compound, Insulin resistance, Internal medicine, Carnitine, Nonalcoholic fatty liver disease, medicine, Humans, Obesity, Morbid, Diacylglycerol kinase, Hepatology, Insulin, Gastroenterology, Settore MED/13 - ENDOCRINOLOGIA, medicine.disease, Obesity, Morbid, Endocrinology, Glucose, chemistry, Liver, Female, Insulin Resistance, Body mass index, medicine.drug, Human
Abstract

Data from studies in animal models indicate that certain lipid metabolites, particularly diacylglycerol, ceramide, and acylcarnitine, disrupt insulin action. We evaluated the relationship between the presence of these metabolites in the liver (assessed by mass spectrometry) and hepatic insulin sensitivity (assessed using a hyperinsulinemic-euglycemic clamp with stable isotope tracer infusion) in 16 obese adults (body mass index, 48 ± 9 kg/m 2 ). There was a negative correlation between insulin-mediated suppression of hepatic glucose production and intrahepatic diacylglycerol (r = −0.609; P = .012), but not with intrahepatic ceramide or acylcarnitine. These data indicate that intrahepatic diacylglycerol is an important mediator of hepatic insulin resistance in obese people with nonalcoholic fatty liver disease.

Published
2012

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