scholarly journals Morbid obesity and type 2 diabetes alter intestinal fatty acid uptake and blood flow

2018 ◽  
Vol 20 (6) ◽  
pp. 1384-1390 ◽  
Author(s):  
Jukka Koffert ◽  
Mia Ståhle ◽  
Henry Karlsson ◽  
Patricia Iozzo ◽  
Paulina Salminen ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Morbid Obesity ◽  
Blood Flow ◽  
Fatty Acid ◽  
Fatty Acid Uptake ◽  
Acid Uptake

Early Effects of Sleeve Gastrectomy (SG) on Systemic and Organ-Specific Dietary Fatty Acid Uptake, Postprandial Free Fatty Acids (FFA), and Glucose Metabolism in Type 2 Diabetes (T2D)

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 150-OR
Author(s):  
ANNE-MARIE CARREAU ◽  
CHRISTOPHE NOLL ◽  
BRIGITTE GUERIN ◽  
LAURENT BIERTHO ◽  
ERIC E. TURCOTTE ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Sleeve Gastrectomy ◽  
Fatty Acid ◽  
Glucose Metabolism ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Organ Specific ◽  
Early Effects

scholarly journals Plasma Free Fatty Acid Uptake and Oxidation Are Already Diminished in Subjects at High Risk for Developing Type 2 Diabetes

Diabetes ◽  
2001 ◽  
Vol 50 (11) ◽  
pp. 2548-2554 ◽  
Author(s):  
M. Mensink ◽  
E. E. Blaak ◽  
M. A. van Baak ◽  
A. J.M. Wagenmakers ◽  
W. H.M. Saris
Keyword(s):  
Type 2 Diabetes ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
High Risk ◽  
Plasma Free Fatty Acid ◽  
Fatty Acid Uptake ◽  
Acid Uptake

scholarly journals Normal Postprandial Nonesterified Fatty Acid Uptake in Muscles Despite Increased Circulating Fatty Acids in Type 2 Diabetes

Diabetes ◽  
2011 ◽  
Vol 60 (2) ◽  
pp. 408-415 ◽  
Author(s):  
S. M. Labbe ◽  
E. Croteau ◽  
T. Grenier-Larouche ◽  
F. Frisch ◽  
R. Ouellet ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Uptake ◽  
Nonesterified Fatty Acid ◽  
Acid Uptake

scholarly journals Fatty acid uptake and blood flow in adipose tissue compartments of morbidly obese subjects with or without type 2 diabetes: effects of bariatric surgery

2017 ◽  
Vol 313 (2) ◽  
pp. E175-E182 ◽  
Author(s):  
Prince Dadson ◽  
Ele Ferrannini ◽  
Linda Landini ◽  
Jarna C. Hannukainen ◽  
Kari K. Kalliokoski ◽  
...  
Keyword(s):  
Blood Flow ◽  
Fatty Acid ◽  
Subcutaneous Fat ◽  
Fatty Acid Uptake ◽  
Morbidly Obese ◽  
Acid Uptake ◽  
Obese Patients ◽  
Subcutaneous Blood Flow ◽  
Obese Subjects

Body fat accumulation, distribution, and metabolic activity are factors in the pathophysiology of obesity and type 2 diabetes (T2D). We investigated adipose blood flow, fatty acid uptake (FAU), and subcutaneous and visceral fat cellularity in obese patients with or without T2D. A total of 23 morbidly obese (mean body mass index = 42 kg/m2) patients were studied before and 6 mo after bariatric surgery; 15 nonobese subjects served as controls. Positron emission tomography was used to measure tissue FAU (with 18F-FTHA) and blood flow (with H215O); MRI was used for fat distribution and fat biopsy for adipocyte size. Obese subjects had subcutaneous hyperplasia and hypertrophy and lower blood flow; when expressed per cell, flow was similar to controls. FAU into subcutaneous and visceral depots was increased in the obese; per unit tissue mass, however, FAU was similar to controls but reduced in skeletal muscle. Fatty acid fractional extraction in subcutaneous fat and muscle was only increased in obese patients with T2D. We conclude that surgery reduces subcutaneous fat hyperplasia and hypertrophy; subcutaneous blood flow and FAU decrease in absolute terms and per cell while fractional FAU remains unchanged in T2D. In the obese, subcutaneous blood flow is a determinant of FAU and is coupled with cellularity; efficiency of FAU is enhanced in subcutaneous fat and muscle in T2D.

Unaltered Fatty Acid Uptake, Utilization, and Mitochondrial Respiration in Right Atrial Appendage of Type 2 Diabetic Human Heart

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 335-OR
Author(s):  
NANDINI RJ ◽  
SR RAJI ◽  
VIVEK V. PILLAI ◽  
JAYAKUMAR K. ◽  
SRINIVAS GOPALA
Keyword(s):  
Fatty Acid ◽  
Mitochondrial Respiration ◽  
Human Heart ◽  
Fatty Acid Uptake ◽  
Atrial Appendage ◽  
Right Atrial ◽  
Acid Uptake ◽  
Right Atrial Appendage ◽  
Type 2 Diabetic

scholarly journals Fatty acid metabolism in obesity and type 2 diabetes mellitus

2003 ◽  
Vol 62 (3) ◽  
pp. 753-760 ◽  
Author(s):  
E. E. Blaak
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Type 2 Diabetes Mellitus ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Acid Oxidation ◽  
Acid Uptake

Disturbances in pathways of lipolysis and fatty acid handling are of importance in the aetiology of obesity and type 2 diabetes mellitus. There is evidence that a lowered catecholamine-mediated lipolytic response may play a role in the development and maintenance of increased adipose tissue stores. Increased adipose tissue stores, a disturbed insulin-mediated regulation of lipolysis and subnormal skeletal muscle non-esterified fatty acid (NEFA) uptake under conditions of high lipolytic rate may increase circulating NEFA concentrations, which may promote insulin resistance and cardiovascular complications. In addition, a disturbance of NEFA uptake by adipose tissue postprandially is also a critical determinant of plasma NEFA concentration. Furthermore, evidence is increasing that insulin-resistant muscle is characterised by a lowered ability to oxidise fatty acids. A dysbalance between fatty acid uptake and fatty acid oxidation may in turn be a factor promoting accumulation of lipid intermediates and triacylglycerols within skeletal muscle, which is strongly associated with skeletal muscle insulin resistance. The present review describes the reported disturbances in pathways of lipolysis and skeletal muscle fatty acid handling, and discusses underlying mechanisms and metabolic consequences of these disturbances.

scholarly journals Postprandial fatty acid uptake and adipocyte remodeling in angiotensin type 2 receptor-deficient mice fed a high-fat/high-fructose diet

Adipocyte ◽  
2015 ◽  
Vol 5 (1) ◽  
pp. 43-52 ◽  
Author(s):  
Christophe Noll ◽  
Sébastien M. Labbé ◽  
Sandra Pinard ◽  
Michael Shum ◽  
Lyne Bilodeau ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
High Fat ◽  
High Fructose Diet ◽  
High Fructose ◽  
Angiotensin Type 2 Receptor ◽  
Deficient Mice ◽  
Angiotensin Type

Thiazolidinediones upregulate impaired fatty acid uptake in skeletal muscle of type 2 diabetic subjects

2003 ◽  
Vol 285 (2) ◽  
pp. E354-E362 ◽  
Author(s):  
Hubertina M. Wilmsen ◽  
Theodore P. Ciaraldi ◽  
Leslie Carter ◽  
Nabeela Reehman ◽  
Sunder R. Mudaliar ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Acid Uptake ◽  
Cd36 Expression ◽  
Palmitate Uptake ◽  
Type 2 Diabetic

We examined the regulation of free fatty acid (FFA, palmitate) uptake into skeletal muscle cells of nondiabetic and type 2 diabetic subjects. Palmitate uptake included a protein-mediated component that was inhibited by phloretin. The protein-mediated component of uptake in muscle cells from type 2 diabetic subjects (78 ± 13 nmol · mg protein-1 · min-1) was reduced compared with that in nondiabetic muscle (150 ± 17, P < 0.01). Acute insulin exposure caused a modest (16 ± 5%, P < 0.025) but significant increase in protein-mediated uptake in nondiabetic muscle. There was no significant insulin effect in diabetic muscle (+19 ± 19%, P = not significant). Chronic (4 day) treatment with a series of thiazolidinediones, troglitazone (Tgz), rosiglitazone (Rgz), and pioglitazone (Pio) increased FFA uptake. Only the phloretin-inhibitable component was increased by treatment, which normalized this activity in diabetic muscle cells. Under the same conditions, FFA oxidation was also increased by thiazolidinedione treatment. Increases in FFA uptake and oxidation were associated with upregulation of fatty acid translocase (FAT/CD36) expression. FAT/CD36 protein was increased by Tgz (90 ± 22% over control), Rgz (146 ± 42%), and Pio (111 ± 37%, P < 0.05 for all 3) treatment. Tgz treatment had no effect on fatty acid transporter protein-1 and membrane-associated plasmalemmal fatty acid-binding protein mRNA expression. We conclude that FFA uptake into cultured muscle cells is, in part, protein mediated and acutely insulin responsive. The basal activity of FFA uptake is impaired in type 2 diabetes. In addition, chronic thiazolidinedione treatment increased FFA uptake and oxidation into cultured human skeletal muscle cells in concert with upregulation of FAT/CD36 expression. Increased FFA uptake and oxidation may contribute to lower circulating FFA levels and reduced insulin resistance in skeletal muscle of individuals with type 2 diabetes following thiazolidinedione treatment.

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