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ffm-fat-free-mass

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Basal palmitate and glucose R<sub>a</sub> in plasma (<em>A</em> and...
Published: 10 July 2020
Figure 1 Basal palmitate and glucose Ra in plasma (A and B) and plasma free fatty acid and glucose concentrations (C and D), insulin-stimulated muscle Rg determined by PET after intravenous injection of [18F]FDG (E), and the relationships between plasma insulin concentration during basal conditions and during the hyperinsulinemic-euglycemic clamp and endogenous glucose Ra in plasma relative to fat-free mass (FFM) (F), total palmitate Ra in plasma (G), and palmitate Ra in plasma relative to fat mass (H) in the lean (n = 8) and obese (n = 8) groups. Data in panels AE are mean ± SEM. *P < 0.05 vs. the lean group. FFM, fat-free mass. Figure 1. Basal palmitate and glucose Ra in plasma (A and B) and plasma free fatty acid and glucose concentrations (C and D), insulin-stimulated muscle Rg determined by PET after intravenous injection of [18F]FDG (E), and the relationships between plasma insulin concentration during basal conditions and during the hyperinsulinemic-euglycemic clamp and endogenous glucose Ra in plasma relative to fat-free mass (FFM) (F), total palmitate Ra in plasma (G), and palmitate Ra in plasma relative to fat mass (H) in the lean (n = 8) and obese (n = 8) groups. Data in panels A–E are mean ± SEM. *P < 0.05 vs. the lean group. FFM, fat-free mass. More
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Relationship between insulin sensitivity (<em>M</em> value) and tot...
Published: 01 May 2004
FIG. 1. Relationship between insulin sensitivity (M value) and total ceramide content in the studied group. ffm, fat-free mass. FIG. 1. Relationship between insulin sensitivity (M value) and total ceramide content in the studied group. ffm, fat-free mass. More
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Absolute changes in visceral <span class="search-highlight">fat</span> (<em>A</em>), intrahepatic lipid (...
Published: 16 October 2012
FIG. 2. Absolute changes in visceral fat (A), intrahepatic lipid (B), and insulin sensitivity (C) for each intervention group. *P values are as compared with the control group (intent-to-treat analyses). FFM, fat-free mass. FIG. 2. Absolute changes in visceral fat (A), intrahepatic lipid (B), and insulin sensitivity (C) for each intervention group. *P values are as compared with the control group (intent-to-treat analyses). FFM, fat-free mass. More
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Basal insulin secretion rate (<em>A</em>) and concentration (<itali
Published: 10 July 2020
Figure 2 Basal insulin secretion rate (A) and concentration (B) and plasma glucose and insulin concentrations and insulin kinetics before and after glucose ingestion (CJ) in the lean (n = 8) and obese (n = 8) groups. Data are mean ± SEM. *P < 0.05 vs. the lean group. FFM, fat-free mass. Figure 2. Basal insulin secretion rate (A) and concentration (B) and plasma glucose and insulin concentrations and insulin kinetics before and after glucose ingestion (C–J) in the lean (n = 8) and obese (n = 8) groups. Data are mean ± SEM. *P < 0.05 vs. the lean group. FFM, fat-free mass. More
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Leg extraction of [3-<sup>3</sup>H]glucose (<em>A</em>) and leg glu...
Published: 01 June 2001
FIG. 10. Leg extraction of [3-3H]glucose (A) and leg glucose uptake (B) observed in the diabetic and nondiabetic subjects during the final 30 min of the study. FFM, fat-free mass. *P < 0.05 vs. nondiabetic subjects. FIG. 10. Leg extraction of [3-3H]glucose (A) and leg glucose uptake (B) observed in the diabetic and nondiabetic subjects during the final 30 min of the study. FFM, fat-free mass. *P < 0.05 vs. nondiabetic subjects. More
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Insulin sensitivity measured by the euglycemic clamp method plotted against...
Published: 01 October 2002
FIG. 3. Insulin sensitivity measured by the euglycemic clamp method plotted against skeletal muscle mitochondrial size measured by electon microscopy. There was a positive correlation between these variables (r = 0.72, P < 0.01). FFM, fat-free mass; Rd, glucose disposal rate. FIG. 3. Insulin sensitivity measured by the euglycemic clamp method plotted against skeletal muscle mitochondrial size measured by electon microscopy. There was a positive correlation between these variables (r = 0.72, P < 0.01). FFM, fat-free mass; Rd, glucose disposal rate. More
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Leg [3-<sup>3</sup>H]glucose extraction (<em>A</em>) and leg glucos...
Published: 01 February 2002
FIG. 7. Leg [3-3H]glucose extraction (A) and leg glucose uptake (B) observed during the final 30 min of the IL/Hep and low- and high-glycerol infusions. *P < 0.001 compared with low- and high-glycerol group. FFM, fat-free mass. FIG. 7. Leg [3-3H]glucose extraction (A) and leg glucose uptake (B) observed during the final 30 min of the IL/Hep and low- and high-glycerol infusions. *P < 0.001 compared with low- and high-glycerol group. FFM, fat-free mass. More
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The correlation between postclamp cathepsin L gene expression and insulin-m...
Published: 01 September 2003
FIG. 5. The correlation between postclamp cathepsin L gene expression and insulin-mediated glucose uptake in the nondiabetic twins (r = 0.70, P = 0.02, n = 10). Cathepsin L mRNA was analyzed using a relative quantitative RT-PCR method and expressed relative to cyclophilin. FFM, fat-free mass. FIG. 5. The correlation between postclamp cathepsin L gene expression and insulin-mediated glucose uptake in the nondiabetic twins (r = 0.70, P = 0.02, n = 10). Cathepsin L mRNA was analyzed using a relative quantitative RT-PCR method and expressed relative to cyclophilin. FFM, fat-free mass. More
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Palmitate R<sub>a</sub> in plasma and plasma palmitate concentration. Basal...
Published: 15 July 2021
Figure 2 Palmitate Ra in plasma and plasma palmitate concentration. Basal palmitate Ra in plasma, an index of adipose tissue lipolytic rate, expressed in relation to fat mass (A) and fat-free mass (B); the relationships between plasma insulin concentration during both basal conditions and the hyperinsulinemic-euglycemic clamp procedure and palmitate Ra in plasma expressed in relation to fat mass (C), fat-free mass (D), and basal plasma palmitate concentration (E); and relationship between palmitate Ra in plasma and plasma palmitate concentration (F) in healthy lean participants and participants with obesity who were grouped, by quartiles, according to insulin-simulated whole-body glucose uptake rate. Values are expressed as mean ± SEM (upward error bar only) or median (IQR). ANOVA was used to evaluate differences in outcome variables among groups in A, B, and E. Skewed data sets were log transformed to achieve normal distribution before analysis. Curve fitting was used to evaluate the relationships between outcome variables in panels C, D, and F. Bars not sharing letters are significantly different from each other, P < 0.05. *Significant main effect of obesity, P < 0.05. FFM, fat-free mass; FM, fat mass; OIR, obese insulin-resistant (Q3/4); OIS, obese insulin-sensitive (Q1). Figure 2. Palmitate Ra in plasma and plasma palmitate concentration. Basal palmitate Ra in plasma, an index of adipose tissue lipolytic rate, expressed in relation to fat mass (A) and fat-free mass (B); the relationships between plasma insulin concentration during both basal conditions and the hyperinsulinemic-euglycemic clamp procedure and palmitate Ra in plasma expressed in relation to fat mass (C), fat-free mass (D), and basal plasma palmitate concentration (E); and relationship between palmitate Ra in plasma and plasma palmitate concentration (F) in healthy lean participants and participants with obesity who were grouped, by quartiles, according to insulin-simulated whole-body glucose uptake rate. Values are expressed as mean ± SEM (upward error bar only) or median (IQR). ANOVA was used to evaluate differences in outcome variables among groups in A, B, and E. Skewed data sets were log transformed to achieve normal distribution before analysis. Curve fitting was used to evaluate the relationships between outcome variables in panels C, D, and F. Bars not sharing letters are significantly different from each other, P < 0.05. *Significant main effect of obesity, P < 0.05. FFM, fat-free mass; FM, fat mass; OIR, obese insulin-resistant (Q3/4); OIS, obese insulin-sensitive (Q1). More
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Increased thermogenesis and energy expenditure in aP2-desnutrin mice. <ital
Published: 09 January 2009
FIG. 7. Increased thermogenesis and energy expenditure in aP2-desnutrin mice. A: Body temperatures of 20-week-old male mice. Temperatures were measured beginning at 10 am following a 17-h overnight fast and before resumption of feeding and were monitored for 24 h (n = 4–6). Inset: Average body temperature (°C) over the day. B: Oxygen consumption rate (Vo2) measured through indirect calorimetry and the average Vo2 over 24 h (inset) (n = 4). *P < 0.05. FFM, fat-free mass. FIG. 7. Increased thermogenesis and energy expenditure in aP2-desnutrin mice. A: Body temperatures of 20-week-old male mice. Temperatures were measured beginning at 10 am following a 17-h overnight fast and before resumption of feeding and were monitored for 24 h (n = 4–6). Inset: Average body temperature (°C) over the day. B: Oxygen consumption rate (Vo2) measured through indirect calorimetry and the average Vo2 over 24 h (inset) (n = 4). *P < 0.05. FFM, fat-free mass. More
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Insulin sensitivity and postprandial glycemic control decline following 1 w...
Published: 29 June 2016
Figure 2 Insulin sensitivity and postprandial glycemic control decline following 1 week of strict bed rest. A: Glucose infusion rates declined by 29 ± 5% following bed rest (P < 0.01). B: Postabsorptive plasma glucose and insulin concentrations on day 1–7 during bed rest. Insulin concentrations increased over time during bed rest (P < 0.001). Postprandial plasma glucose and insulin concentrations in the meal tolerance tests pre– and post–bed rest are depicted in C and D, respectively. For glucose, no changes in iAUC were observed (P > 0.05), whereas iAUC for insulin were increased following bed rest (P < 0.05). FFM, fat-free mass. Data are shown as mean ± SEM. *Significantly different from pre–bed rest value (P < 0.05). Figure 2. Insulin sensitivity and postprandial glycemic control decline following 1 week of strict bed rest. A: Glucose infusion rates declined by 29 ± 5% following bed rest (P < 0.01). B: Postabsorptive plasma glucose and insulin concentrations on day 1–7 during bed rest. Insulin concentrations increased over time during bed rest (P < 0.001). Postprandial plasma glucose and insulin concentrations in the meal tolerance tests pre– and post–bed rest are depicted in C and D, respectively. For glucose, no changes in iAUC were observed (P > 0.05), whereas iAUC for insulin were increased following bed rest (P < 0.05). FFM, fat-free mass. Data are shown as mean ± SEM. *Significantly different from pre–bed rest value (P < 0.05). More
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Modulation of first-phase insulin secretion, as acute insulin secretion res...
Published: 11 December 2017
Figure 7 Modulation of first-phase insulin secretion, as acute insulin secretion response (AISR) during an IVGTT, with insulin resistance or basal hyperglycemia. AISR is calculated as the mean secretion increment above basal. A: Relationship between AISR and insulin sensitivity in subjects with normal glucose tolerance (data from Mari et al. [ 20 ]). The dots are the experimental data. The model simulation (line) shows AISR in the quartiles of insulin sensitivity and is obtained by gradually shifting upward the refilling function (fr) (right) so that basal insulin secretion is increased to match the values experimentally determined in the quartiles. The refilling function is plotted as a function of calcium concentration (C) at a glucose concentration (G) of 10 mmol/L, and the gray shading shows how the refilling function is increased with insulin resistance. B: Relationship between AISR and basal glucose in subjects with glucose tolerance spanning from normal to T2D (data from Mari et al. [ 21 ]). The dots are the experimental data. The model simulation (line) is obtained at a basal glucose ranging from 5.0 to 8.0 mmol/L in steps of 0.5 mmol/L. For each basal glucose level, the slope of the refilling function (right) is progressively decreased to simulate a defective amplifying pathway with hyperglycemia. The refilling function (right) is plotted as a function of intracellular calcium concentration at a glucose concentration of 10 mmol/L; the gray shading shows how the refilling function is flattened with hyperglycemia. More details on these simulations are provided in the Supplementary Data . FFM, fat-free mass. Figure 7. Modulation of first-phase insulin secretion, as acute insulin secretion response (AISR) during an IVGTT, with insulin resistance or basal hyperglycemia. AISR is calculated as the mean secretion increment above basal. A: Relationship between AISR and insulin sensitivity in subjects with normal glucose tolerance (data from Mari et al. [20]). The dots are the experimental data. The model simulation (line) shows AISR in the quartiles of insulin sensitivity and is obtained by gradually shifting upward the refilling function (fr) (right) so that basal insulin secretion is increased to match the values experimentally determined in the quartiles. The refilling function is plotted as a function of calcium concentration (C) at a glucose concentration (G) of 10 mmol/L, and the gray shading shows how the refilling function is increased with insulin resistance. B: Relationship between AISR and basal glucose in subjects with glucose tolerance spanning from normal to T2D (data from Mari et al. [21]). The dots are the experimental data. The model simulation (line) is obtained at a basal glucose ranging from 5.0 to 8.0 mmol/L in steps of 0.5 mmol/L. For each basal glucose level, the slope of the refilling function (right) is progressively decreased to simulate a defective amplifying pathway with hyperglycemia. The refilling function (right) is plotted as a function of intracellular calcium concentration at a glucose concentration of 10 mmol/L; the gray shading shows how the refilling function is flattened with hyperglycemia. More details on these simulations are provided in the Supplementary Data. FFM, fat-free mass. More
Journal Articles
Journal: Diabetes
Diabetes 1990;39(2):149–156
Published: 01 February 1990
... uptake was matched at ∼8 mg · kg−1 fat-free mass (FFM) · min1 with primarily hyperinsulinemia (1350 ± 445 pM) or hyperglycemia (20.8 ± 1.8 mM), identical rates of glucose oxidation (3.21 ± 0.29 and 3.10 ± 0.23 mg · kg−1 FFM · min−1, NS) and nonoxidative glucose metabolism...
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<em>A</em>: Key differences and similarities in chronic glycemia an...
Published: 13 April 2020
Figure 1 A: Key differences and similarities in chronic glycemia and insulin distribution affecting insulin sensitivity between participant groups. Pe. hyperinsulinemia, peripheral hyperinsulinemia. B: Scatterplot depicting correlation between mean basal insulin concentration (x-axis), glycosylated hemoglobin (HbA1c, darker shade of blue represents higher HbA1c), and mean rate of glucose disposal (Rd) during hyperinsulinemic, euglycemic clamp. Insulin was infused at 40 mU/m2/min when Rd was measured. The figure shows that participants with type 1 diabetes (T1DM) (squares) had higher basal insulinemia (further to the right on the x-axis), higher chronic glycemia (darker shade of blue), and lower Rd (further down on the y-axis). GCK-MODY participants (triangles) had glycemia similar to that of T1DM participants (similar shade of blue) but lower insulinemia (further to the left on the x-axis) and higher Rd (further up on the y-axis). Despite having differing glycemia (differing shades of blue), GCK-MODY and control (circles) participants generally had lower and similar insulinemia and higher Rd than T1DM participants. Coefficient of determination (R2) between basal insulin concentration and Rd was 0.36. R2 between HbA1c and Rd was 0.09. R2 for the multivariable linear regression model including both basal insulin concentration and HbA1c as dependent variables and Rd as an independent variable was 0.36. Thus, these linear regression analyses show that insulinemia alone explained 36% of the variance in Rd, a factor that was virtually unchanged with the addition of chronic glycemia in multivariable linear regression analysis. Collectively, these data suggest hyperinsulinemia stemming from peripheral insulin delivery plays a far greater role than hyperglycemia in causing peripheral insulin resistance in type 1 diabetes. FFM, fat-free mass. Figure 1. A: Key differences and similarities in chronic glycemia and insulin distribution affecting insulin sensitivity between participant groups. Pe. hyperinsulinemia, peripheral hyperinsulinemia. B: Scatterplot depicting correlation between mean basal insulin concentration (x-axis), glycosylated hemoglobin (HbA1c, darker shade of blue represents higher HbA1c), and mean rate of glucose disposal (Rd) during hyperinsulinemic, euglycemic clamp. Insulin was infused at 40 mU/m2/min when Rd was measured. The figure shows that participants with type 1 diabetes (T1DM) (squares) had higher basal insulinemia (further to the right on the x-axis), higher chronic glycemia (darker shade of blue), and lower Rd (further down on the y-axis). GCK-MODY participants (triangles) had glycemia similar to that of T1DM participants (similar shade of blue) but lower insulinemia (further to the left on the x-axis) and higher Rd (further up on the y-axis). Despite having differing glycemia (differing shades of blue), GCK-MODY and control (circles) participants generally had lower and similar insulinemia and higher Rd than T1DM participants. Coefficient of determination (R2) between basal insulin concentration and Rd was 0.36. R2 between HbA1c and Rd was 0.09. R2 for the multivariable linear regression model including both basal insulin concentration and HbA1c as dependent variables and Rd as an independent variable was 0.36. Thus, these linear regression analyses show that insulinemia alone explained 36% of the variance in Rd, a factor that was virtually unchanged with the addition of chronic glycemia in multivariable linear regression analysis. Collectively, these data suggest hyperinsulinemia stemming from peripheral insulin delivery plays a far greater role than hyperglycemia in causing peripheral insulin resistance in type 1 diabetes. FFM, fat-free mass. More
Journal Articles
Journal: Diabetes
Diabetes 1990;39(1):22–30
Published: 01 January 1990
... to compare Gox, Nox, and Fox at two different rates of glucose uptake (∼7 and 10 mg · kg−1 fat-free mass [FFM] · min−1) matched at each level by either hyperglycemia or hyperinsulinemia. When glucose uptake was matched...
Meeting Abstracts
Journal: Diabetes
Diabetes 1998;47(11):1757–1762
Published: 01 November 1998
... levels correlated with BMI (r = 0.50, P = 0.002), fat-free mass (FFM) (r = 0.61, P < 0.0001), and waist-to-hip ratio (WHR) (r = 0.39, P = 0.02), but not with fat mass or percent fat mass. sTNFR2 levels correlated with basal glucose levels (r = 0.45, P = 0.007), area under the curve (AUC) for glucose...
Meeting Abstracts
Journal: Diabetes
Diabetes 2000;49(12):2102–2107
Published: 01 December 2000
...(-1) fat-free mass [FFM] x min(-1) and control 15.8 +/- 1.8 vs. 28.6 +/- 2.1 micromol x kg(-1) FFM x min(-1)). The oxidation of plasma-derived fatty acids was significantly lower in type 2 diabetic subjects during both conditions (P < 0.05, baseline vs. exercise [40-60 min]; type 2 diabetes 4.2...
Journal Articles
Journal: Diabetes
Diabetes 1988;37(2):154–159
Published: 01 February 1988
... gluconeogenesis appears to account for a sub- rate of recycling) decreased in the diabetic subjects from 3.80 to 2.74 mg min~1 k g 1 fat-free mass (FFM) (P ...
Journal Articles
Journal: Diabetes
Diabetes 1994;43(7):908–914
Published: 01 July 1994
... by using indirect respiratory calorimetry. Basal glycerol rate of appearance (Rα; lipolysis) and fat oxidation were similar between prepubertal and pubertal subjects but higher than adults when the data were expressed per kilogram body weight or per kilogram fat-free mass (FFM; glycerol...
Journal Articles
Journal: Diabetes
Diabetes 2003;52(9):2191–2197
Published: 01 September 2003
... improved by 19%, from 38.8 ± 1.2 to 46.0 ± 1.0 ml · kg fat-free mass (FFM)−1 · min−1 (P < 0.05). Insulin sensitivity improved 49 ± 10% (6.70 ± 0.40 to 9.51 ± 0.51 mg · min−1 · kg FFM−1; P < 0.05). Rates of fat oxidation following...