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M Beylot

Publications and source records attributed to M Beylot.

107 records · Page 6Linked to original sources

Regulation of ketonaemia in hyperthyroidism: study of the role of free fatty acids.

We have indirectly assessed the role of free fatty acids (FFA) and of hepatic ketogenesis in the regulation of ketone body levels in euthyroid and hyperthyroid subjects. All studies were performed under controlled dietary conditions (35 and 45 kcal/kg body weight/day respectively for euthyroid and hyperthyroid subjects). In the post-absorptive state hyperthyroid patients had normal, glucagon levels and, in spite of increased insulinemia (p less than 0.02), elevated concentrations of blood glucose (p less than 0.01), glycerol (p less than 0.001) and ketone bodies (p less than 0.05). In the face of this hyperketonaemia, there was no significant increase of plasma FFA, suggesting possible increased hepatic conversion of FFA to ketone bodies. However, when FFA were acutely raised to high levels, the induced rise of ketone bodies was similar in hyperthyroid and euthyroid subjects. Oral propranolol administration to hyperthyroid patients in the post-absorptive state decreased the concentrations of glycerol (p less than 0.05) and ketone bodies (p less than 0.05) without altering insulin concentrations. Ketone bodies fell without any significant decrease of FFA suggesting a possible direct effect of propranolol administration on hepatic ketogenesis. However, the ketone body response to raised FFA levels was unaffected by propranolol. We have evidence in hyperthyroid patients of increased lipolysis and ketogenesis in spite of increased daily caloric intake. These results suggest that these metabolic abnormalities are not merely due to relative starvation. We have tentative evidence for modification of the intra-hepatic conversion of FFA to ketone bodies in the post-absorptive state but no supporting evidence when FFA levels were experimentally raised.

Adult↗

[Serum lipids in diabetes mellitus. Relation to equilibration and microangiopathy].

We have determined in 128 diabetic (57 non insulin-dependent (NIDDM) and 71 insulin-dependent (IDDM) patients) and in control subjects, serum total cholesterol, HDL cholesterol, triglycerides and Hb Alc levels. Presence of macroangiopathy was assessed by clinical findings. In IDDM increasingly poor control of diabetes was associated with significant increases in total cholesterol (p less than 0.001) and triglycerides (p less than 0.01). HDL cholesterol (1.19 +/- 0.39 mM/l) did not differ from control subjects (1.30 +/- 0.35 mM/l) and was not related to Hb Alc levels. NIDDM had increased total cholesterol (5.91 +/- 1.45 vs 5.38 +/- 0.93 mM/l, p less than 0.05) and triglycerides (2.06 - 0.32 to 8.80- vs 1.03 - 0.22 à 2.20 mM/l, p less than 0.01) and decreased HDL cholesterol (1.08 +/- 0.44 vs 1.31 +/- 0.36 mM/l, p less than 0.01). These differences could be explained only in part by the overweight of the NIDDM patients. There was no significant correlation in NIDDM between Hb Alc and serum lipids levels but overweight and triglycerides were positively correlated (p less than 0.02) and triglycerides and HDL cholesterol negatively correlated (p less than 0.05). IDDM with macroangiopathy had higher total cholesterol levels than those without (6.44 +/- 1.60 vs 5.29 +/- 1.22 mM/l, p less than 0.01). IDDM and NIDDM with macroangiopathy had slightly decreased HDL cholesterol; however, the diabetic subjects with macroangiopathy were older and had a longer duration of diabetes than subjects without macroangiopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Abnormalities of heart rate and arterial blood pressure regulation in diabetes mellitus. Relation with age, duration of diabetes and presence of peripheral neuropathy.

We have determined in 46 control subjects and 117 diabetic patients with or without peripheral neuropathy (PN) the blood pressure response to standing and the heart rate variations during deep breathing (HRV) and standing (T/B ratio). HRV was abnormal in 20% of diabetics and T/B ratio only in 8%. HRV and T/B ratio decreased with age both in control and diabetic group and significant alterations of these two tests in diabetic patients were found only for the youngest subjects; HRV and T/B ratio were not related to the duration of diabetes. Ten diabetics had orthostatic hypotension. Diabetics with PN had lower HRV and T/B ratio than the others and, excluding the 10 subjects with large orthostatic hypotension, a lack of increase in diastolic blood pressure and a transient fall in systolic blood pressure on standing. T/B ratio appears in our subjects of less value than HRV for the diagnosis of cardiac autonomic neuropathy; because of the spontaneous alterations with age of the response to these tests interpretation of the results in diabetics is possible only in the presence of appropriate data in control subjects. PN in diabetic patients is strongly associated with abnormalities of heart rate regulation suggestive of cardiac vagal neuropathy and with abnormalities of blood pressure regulation suggestive of peripheral sympathetic lesions.

Adolescent↗

[Effects of propranolol and indomethacin upon urinary hydroxyproline in hyperthyroid patients (author's transl)].

Hydroxyproline excretion was increased by hyperthyroid patients. This increase was related to thyroid hormone levels. Propranolol administration induced a decrease in hydroxyproline excretion and in immunoreactive triiodothyronine. Indometacin administration induced a decrease in urinary excretion of prostaglandins but had no effect on hydroxyproline excretion. These data suggest that the increased bone resorption of hyperthyroidism may involve a catecholamine beta receptor-dependent mechanism and is probably independent of prostaglandins.

Adult↗

Ultrasonographic determination of residual urine in diabetic subjects: relationship to neuropathy and urinary tract infection.

The presence of residual urine was determined by postvoid bladder ultrasonography in 37 control subjects and 102 unselected insulin-dependent and non-insulin-dependent diabetic patients. Significant residual volume was detected in 19 diabetic subjects without explanation other than diabetic neurogenic bladder dysfunction in 15. The four others had prostatic hypertrophy. Excluding these four subjects, those with residual urine were slightly older than the others (P less than 0.05), but the known duration of diabetes was increased only for the insulin-dependent group (P less than 0.05). The presence of residual urine was strongly associated with peripheral neuropathy (P less than 0.001). In contrast, of all the manifestations of autonomic failure studied, only impotence (P less than 0.01) and decreased pupil motility (P less than 0.05) were associated with residual urine. The prevalence of urinary tract infection was higher in women than in men (P less than 0.02). This prevalence was increased in the presence of residual urine (P less than 0.02) but only for men (P less than 0.001).

Adult↗

[New research techniques in human nutrition].

Accurate determination of energy requirement and nutrients metabolism is essential to improve physiological knowledge and for physiopathological purpose in human nutrition. This evaluation is an absolute necessity for food industry. Energy expenditure could be precisely determined by indirect calorimetry or doubly labeled water technic. Nutrients metabolism and substrates turn-over studies are now accessible without health hazard using tracers labelled with stable isotopes. These three methods are the basic tools for the new Research Nutrition Center which are now in progress.

Calorimetry, Indirect↗

Effects of small variations in insulin and glucagon levels on plasma aminoacids concentrations.

To determine the effect in normal subjects of small variations of insulin and glucagon on plasma aminoacids concentrations we suppressed endocrine pancreas secretion with somatostatin and measured aminoacids levels during a sequential insulin infusion in the absence (control test, low glucagon level) or in the presence (normal glucagon concentration) of a replacement glucagon infusion. Insulin infusion rates were 0.05, 0.09, 0.15 and 0.30 mU.kg-1.min-1 during the control test and 0.09, 0.15, 0.30 and 0.40 mU.kg-1.min-1 during the replacement test. During the control test, glucagon decreased (p less than 0.01) and insulin levels were successively 8.2 +/- 0.4, 10.1 +/- 0.7, 11.9 +/- 0.14 and 18.5 +/- 0.8 mU.l-1. The only effect on insulin was to decrease branched-chain aminoacids (BCAA). BCAA were inversely related to insulinemia (p less than 0.01). A significant decrease was obtained for an insulin level of 11.9 +/- 0.4 mU.l-1, a value intermediate between those decreasing glycerol (10.1 +/- 0.7 mU.l-1) and stimulating total body glucose uptake (18.5 +/- 0.8 mU.l-1). During the test with glucagon replacement glucagon was maintained at its initial value. Insulin levels were successively 8.3 +/- 0.3, 11.9 +/- 0.3, 19.7 +/- 0.6 and 26.7 +/- 0.5 mU.l-1. Insulin decreased always BCAA but also threonine, proline, tyrosine, methionine and total aminoacid levels. BCAA were always inversely related to insulin levels (p less than 0.01) but the slope of the relationship was modified and more insulin was needed to decrease BCAA concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Metabolic studies in lipoatrophic diabetes: mechanism of hyperglycemia and evidence of resistance to insulin of lipid metabolism.

We determined in 5 control subjects and in one patient with total congenital lipoatrophy (LA) the effect of insulin infusion on glucose flux and some aspects of lipid metabolism. In the post-absorptive state LA had moderate hyperglycemia (9.2 versus 3.80 +/- 0.07 mmol.l-1) and hyperinsulinemia (19 vs 12 +/- 3 mU.l-1) and a massive increase in glucose production (7.51 mg.kg.-1.min-1) and disappearance (7.40 mg.kg-1.min-1) rates (control subjects: 2.29 +/- 0.14 mg.kg-1 min-1). Raising peripheral insulin levels to 28 +/- 3 mU.l-1 suppressed endogenous glucose production in the control subjects whereas in LA significant (2.01 mg.kg-1.min-1) production persisted even when peripheral insulinemia was raised to 58 mU.l-1. Insulin infusion in control subjects increased progressively glucose utilization to a final value of 15.7 +/- 0.7 mg.kg-1.min-1 (corresponding plasma insulin: 482 +/- 44 mU.l-1). Insulin infusion in LA initially lowered glucose level near to normal values and exogenous glucose was infused for an insulin infusion rate of 10 mU.kg-1.min-1; at this insulin infusion rate glucose utilization rate (6.52 mg.kg-1.min-1) was decreased relative to control subjects in spite of higher insulin levels (750 mU.l-1). NEFA, glycerol and ketone bodies (KB) levels were decreased to undetectable levels by insulin infusion in the normal subjects whereas NEFA and glycerol were decreased only in part and KB were not modified in LA. In addition glycerol and KB appearance rates determined in LA were not suppressed by insulin infusion as expected.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Insulin-mediated glucose disposal in type 1 (insulin-dependent) diabetic subjects treated by continuous subcutaneous or intraperitoneal insulin fusion.

In order to determine if intraperitoneal insulin infusion could improve the insulin resistance of type 1 diabetic patients we have used the englycaemic insulin clamp technique in order to study the effects of insulin on glucose disposal in four C peptide negative type 1 diabetic patients treated by continuous subcutaneous or intraperitoneal insulin infusion and in five control subjects. Compared to control subjects, the diabetic patients treated by subcutaneous insulin infusion had a decreased maximal capacity of glucose utilization (diabetics: 12.6 +/- 0.3 mg.kg-1.min-1; controls: 15.7 +/- 0.7 mg/kg-1.min-1, p less than 0.01) and a trend towards higher half-maximally effective insulin concentrations (diabetics: 70 +/- 11 mU/l-1, controls: 48 +/- 4 mU/l-1). Treatment of the diabetic patients by intraperitoneal insulin infusion for 2 months decreased their mean peripheral free insulin levels (during subcutaneous infusion: 23.5 +/- 2.2 mU/l-1; during intraperitoneal infusion: 18.4 +/- 1.4 mU/l-1, p less than 0.05). However, mean daily insulin requirements were not decreased (during subcutaneous infusion: 0.59 +/- 0.05 U/kg-1.day-1; during intraperitoneal infusion: 0.57 +/- 0.03 U/kg-1.min-1). Moreover, the diabetic patients had a consistently lower maximal capacity of glucose utilization (12.6 +/- 0.7 mg kg-1.min-1) than control subjects (p less than 0.01) without modification of the half-maximally effective insulin concentration (62 +/- 10 mU.l-1). In conclusion, the only benefit of intraperitoneal insulin infusion was a reduction of peripheral free insulin levels; this decrease of peripheral insulinaemia was not associated with an improvement in the insulin resistance of diabetic patients.

Adult↗

[Absence of effect of propranolol on urinary excretion of 3-methylhistidine in hyperthyroidism].

Lean body mass and muscle protein breakdown were evaluated in euthyroid and hyperthyroid subjects by measuring the urinary excretion of creatinine and 3-methylhistidine. Since catecholamines probably have an inhibitory effect on muscle protein catabolism through a beta-receptor mechanism, the effects of propranolol on 3-methylhistidine excretion were also evaluated in hyperthyroid subjects. Hyperthyroid subjects had a lower lean body mass (34.9 +/- 6.3 kg versus 47.7 +/- 8.9 kg, p less than 0.001) and a greater 3-methylhistidine excretion (25.1 +/- 7.4 versus 19.0 +/- 4.8 mumol/mmol creatinine, p less than 0.05) than euthyroid subjects. Propranolol administered orally to hyperthyroid subjects decreased pulse rate (p less than 0.01) and plasma triiodothyronine concentrations (from 5.40 +/- 2.28 to 3.61 +/- 1.61 nmol/l, p less than 0.01), but did not modify urinary 3-methylhistidine excretion (24.8 +/- 8.7 versus 25.1 +/- 7.4 mumol/mmol creatinine). These results suggest that muscle wasting in hyperthyroidism is related to increased protein catabolism. This increased protein breakdown is not modified by short term administration of propranolol, a beta-blocking agent widely used in the management of hyperthyroidism.

Adult↗

[Effect of thyroid function on ketogenesis (author's transl)].

Thyroid hormone effects have been studied in both rats and human. In rats ketone body levels are increased by thyroid hormone excess at the initial phase of starvation. Glucose levels are also increased at the initial and late phase of starvation. Ketone bodies production of isolated liver cells from thyroidectomized fed rats (14 +/- 0,2 muMol/g/h) are decreased when compared with cells from thyroidectomized fed rats treated with triiodothyronine 63 +/- 3 muMol/g/h). These changes are related to a direct effect of T3. Ketone bodies levels are increased in Grave's diseases. The increase is significantly correlated to thyroid hormone levels.

Animals↗