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Basal and insulin mediated VLDL-triglyceride kinetics in type 2 diabetic men.

Sørensen LP, Andersen IR, Søndergaard E, Gormsen LC, Schmitz O, Christiansen JS, Nielsen S - Diabetes (2010)

Bottom Line: VLDL-TG secretion was significantly greater in diabetic compared with healthy men (basal: 86.9 [31.0] vs. 61.9 [30.0] μmol/min, P = 0.03; clamp: 60.0 [26.2] vs. 34.2 [17.9] μmol · min⁻¹, P = 0.01).Basal VLDL-TG storage was similar, but significantly greater in abdominal compared with leg fat.During hyperinsulinemia VLDL-TG FA oxidation is significantly increased in proportion of EE in type 2 diabetic men.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology and Internal Medicine, University Hospital, Aarhus, Denmark.

ABSTRACT

Objective: Increased very-low-density lipoprotein triglycerides (VLDL-TG) concentration is a central feature of diabetic dyslipidemia. The objective was to compare basal and insulin mediated VLDL-TG kinetics, oxidation, and adipose tissue storage in type 2 diabetic and healthy (nondiabetic) men.

Research design and methods: Eleven type 2 diabetic and 11 healthy men, matched for BMI and age, were included. Ex vivo-labeled VLDL-TG tracers, blood and breath samples, fat biopsies, indirect calorimetry, and body composition measures were applied to determine VLDL-TG kinetics, VLDL-TG fatty acids (FA) oxidation, and storage in regional adipose tissue before and during a hyperinsulinemic euglycaemic clamp.

Results: VLDL-TG secretion was significantly greater in diabetic compared with healthy men (basal: 86.9 [31.0] vs. 61.9 [30.0] μmol/min, P = 0.03; clamp: 60.0 [26.2] vs. 34.2 [17.9] μmol · min⁻¹, P = 0.01). The insulin mediated suppression of VLDL-TG secretion was significant in both groups. VLDL-TG clearance was lower in diabetic men (basal: 84.6 [32.7] vs. 115.4 [44.3] ml · min⁻¹, P = 0.08; clamp: 76.3 [30.6] vs. 119.0 [50.2] ml · min⁻¹, P = 0.03). During hyperinsulinemia fractional VLDL-TG FA oxidation was comparable, but in percentage of energy expenditure (EE), significantly higher in diabetic men. Basal VLDL-TG storage was similar, but significantly greater in abdominal compared with leg fat.

Conclusions: Increased VLDL-TG in type 2 diabetic men is caused by greater VLDL-TG secretion and less so by lower VLDL-TG clearance. The ability of hyperinsulinemia to suppress VLDL-TG secretion appears preserved. During hyperinsulinemia VLDL-TG FA oxidation is significantly increased in proportion of EE in type 2 diabetic men. Greater basal abdominal VLDL-TG storage may help explain the accumulation of upper-body fat in insulin-resistant individuals.

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Storage of VLDL-TG FA in abdominal (A and B) and leg (C and D) subcutaneous adipose tissue expressed as fraction of VLDL-TG secretion (A and C) and as storage rate (fraction storage × VLDL secretion rate) (B and D). Black bars, healthy subjects; white bars, type 2 diabetic subjects. Data are presented as mean ± SEM.
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Figure 5: Storage of VLDL-TG FA in abdominal (A and B) and leg (C and D) subcutaneous adipose tissue expressed as fraction of VLDL-TG secretion (A and C) and as storage rate (fraction storage × VLDL secretion rate) (B and D). Black bars, healthy subjects; white bars, type 2 diabetic subjects. Data are presented as mean ± SEM.

Mentions: At 120 min (4 h after bolus infusion of [9,10-3H]VLDL-TG), the remaining 3H plasma activity was (6.1 [2.2–20.1]% vs. 5.8 [2.3–8.0], ns, diabetic vs. healthy men, respectively). This was calculated by dividing plasma 3H activity (dpm · ml−1) at 120 min by the initial activity estimated by dividing infused activity (dpm) by plasma volume (55 ml · kg FFM−1) (24). Fractional VLDL-TG FA storage was comparable in the groups both in abdominal (4.2 [2.9] vs. 4.2 [2.3]%, ns) and leg fat (1.0 [0.3–4.8 ] vs. 0.8 [0.2–5.5]%, ns) but significantly greater in abdominal compared with leg fat (Fig. 5). Since practically all 3H activity had disappeared from plasma at 120 min, it is possible to estimate the rate of VLDL-TG FA storage in the tissues by multiplying fractional storage by turnover rate. Despite the difference in VLDL-TG secretion rate, there was no significant difference between diabetic and healthy men in VLDL-TG FA storage rate in abdominal (2.7 [1.3–7.0 ] vs. 2.0 [0.5–5.6 ] μmol · min−1, ns) or in leg fat (1.0 [0.2–3.4 ] vs. 0.4 [0.1–4.7 ] μmol · min−1, ns). However, storage rate was significantly greater in abdominal fat compared with leg fat in both groups (Fig. 5).


Basal and insulin mediated VLDL-triglyceride kinetics in type 2 diabetic men.

Sørensen LP, Andersen IR, Søndergaard E, Gormsen LC, Schmitz O, Christiansen JS, Nielsen S - Diabetes (2010)

Storage of VLDL-TG FA in abdominal (A and B) and leg (C and D) subcutaneous adipose tissue expressed as fraction of VLDL-TG secretion (A and C) and as storage rate (fraction storage × VLDL secretion rate) (B and D). Black bars, healthy subjects; white bars, type 2 diabetic subjects. Data are presented as mean ± SEM.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3012201&req=5

Figure 5: Storage of VLDL-TG FA in abdominal (A and B) and leg (C and D) subcutaneous adipose tissue expressed as fraction of VLDL-TG secretion (A and C) and as storage rate (fraction storage × VLDL secretion rate) (B and D). Black bars, healthy subjects; white bars, type 2 diabetic subjects. Data are presented as mean ± SEM.
Mentions: At 120 min (4 h after bolus infusion of [9,10-3H]VLDL-TG), the remaining 3H plasma activity was (6.1 [2.2–20.1]% vs. 5.8 [2.3–8.0], ns, diabetic vs. healthy men, respectively). This was calculated by dividing plasma 3H activity (dpm · ml−1) at 120 min by the initial activity estimated by dividing infused activity (dpm) by plasma volume (55 ml · kg FFM−1) (24). Fractional VLDL-TG FA storage was comparable in the groups both in abdominal (4.2 [2.9] vs. 4.2 [2.3]%, ns) and leg fat (1.0 [0.3–4.8 ] vs. 0.8 [0.2–5.5]%, ns) but significantly greater in abdominal compared with leg fat (Fig. 5). Since practically all 3H activity had disappeared from plasma at 120 min, it is possible to estimate the rate of VLDL-TG FA storage in the tissues by multiplying fractional storage by turnover rate. Despite the difference in VLDL-TG secretion rate, there was no significant difference between diabetic and healthy men in VLDL-TG FA storage rate in abdominal (2.7 [1.3–7.0 ] vs. 2.0 [0.5–5.6 ] μmol · min−1, ns) or in leg fat (1.0 [0.2–3.4 ] vs. 0.4 [0.1–4.7 ] μmol · min−1, ns). However, storage rate was significantly greater in abdominal fat compared with leg fat in both groups (Fig. 5).

Bottom Line: VLDL-TG secretion was significantly greater in diabetic compared with healthy men (basal: 86.9 [31.0] vs. 61.9 [30.0] μmol/min, P = 0.03; clamp: 60.0 [26.2] vs. 34.2 [17.9] μmol · min⁻¹, P = 0.01).Basal VLDL-TG storage was similar, but significantly greater in abdominal compared with leg fat.During hyperinsulinemia VLDL-TG FA oxidation is significantly increased in proportion of EE in type 2 diabetic men.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology and Internal Medicine, University Hospital, Aarhus, Denmark.

ABSTRACT

Objective: Increased very-low-density lipoprotein triglycerides (VLDL-TG) concentration is a central feature of diabetic dyslipidemia. The objective was to compare basal and insulin mediated VLDL-TG kinetics, oxidation, and adipose tissue storage in type 2 diabetic and healthy (nondiabetic) men.

Research design and methods: Eleven type 2 diabetic and 11 healthy men, matched for BMI and age, were included. Ex vivo-labeled VLDL-TG tracers, blood and breath samples, fat biopsies, indirect calorimetry, and body composition measures were applied to determine VLDL-TG kinetics, VLDL-TG fatty acids (FA) oxidation, and storage in regional adipose tissue before and during a hyperinsulinemic euglycaemic clamp.

Results: VLDL-TG secretion was significantly greater in diabetic compared with healthy men (basal: 86.9 [31.0] vs. 61.9 [30.0] μmol/min, P = 0.03; clamp: 60.0 [26.2] vs. 34.2 [17.9] μmol · min⁻¹, P = 0.01). The insulin mediated suppression of VLDL-TG secretion was significant in both groups. VLDL-TG clearance was lower in diabetic men (basal: 84.6 [32.7] vs. 115.4 [44.3] ml · min⁻¹, P = 0.08; clamp: 76.3 [30.6] vs. 119.0 [50.2] ml · min⁻¹, P = 0.03). During hyperinsulinemia fractional VLDL-TG FA oxidation was comparable, but in percentage of energy expenditure (EE), significantly higher in diabetic men. Basal VLDL-TG storage was similar, but significantly greater in abdominal compared with leg fat.

Conclusions: Increased VLDL-TG in type 2 diabetic men is caused by greater VLDL-TG secretion and less so by lower VLDL-TG clearance. The ability of hyperinsulinemia to suppress VLDL-TG secretion appears preserved. During hyperinsulinemia VLDL-TG FA oxidation is significantly increased in proportion of EE in type 2 diabetic men. Greater basal abdominal VLDL-TG storage may help explain the accumulation of upper-body fat in insulin-resistant individuals.

Show MeSH
Related in: MedlinePlus