Summary
Basal heart triacylglycerol (TG) (μmole triacylglycerol/g of dry weight) (- before
“in vitro” Langendorff perfusion -) was significantly higher in animals rendered chronically
hypertriglyceridaemic (H) by a 63% sucrose-rich diet than in controls (C, standard
diet); 28 ± 2.6 X ± SEM vs. 19.3 ± 1.2; respectively (p < 0.01). After 40′ perfusion
with Krebs-Henseleit buffer + 5.5 mM glucose, 2.5 mM Ca++, TG content fell to 14.2 ± 0.6 in C and 14.9 ± 1.9 in H (n.s.). Administration of
1 nmol × min-1 of glucagon (Gn) from min 20 to 40 reduced TG to 9.0 ± 0.5 in C (p < 0.05). In contrast
no effect of Gn was observed in H (TG at min 40: 16.7 ± 2.5). Glycogen (Gly) content
(μmol/g of dry weight) after Gn perfusion fell from 30 ± 1.9 to 17 ± 2.1 (p < 0.01)
in C, while again no effect was recorded in H. “In vivo” plasma glucose fractional
coefficient disappearance rate was lower (p < 0.001) in H: 1.01 × 10-2 ± 0.09 × 10-2 vs 2.61 × 10-2 ± 0.14 × 10-2 in C, in spite of H showing hyperinsulin secretion. Hyperinsulinism was further documented
by “in vitro” Iri release studies from incubated pancreas pieces. In the absence of
glucose (G) from the incubation medium H produced 541 ± 19.8 mU/mg weight tissue/20′,
while C produced 91.2 ± 12.7 (p < 0.001). With 100 mg% G, H released 1058 ± 259 and
C 377 ± 82.5 (p < 0.001). It is suggested that hyperinsulin secretion plus insulin
resistance may account for the above findings.
Key-Words:
Hypertriglyceridemia
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Sucrose-Rich Diet
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Glucagon
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Hyperinsulinism
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Triglyceride Metabolism
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Heart Triglyceride
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Glucose Intolerance
