[Corticotropin deficiency and hyporeninism-hypoaldosteronism].
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Adrenocorticotropic Hormone↗
Biomedical subjects
H Gin
Publications and source records attributed to H Gin.
Low protein diet in uremia: effects on glucose metabolism and energy production rate.
Low-protein diets (LPD) increase insulin-mediated glucose disposal in chronic renal failure (CRF), but the fate of the better utilized glucose and the effect on energy production rate are unknown. Using a two-step (1 and 5 mU x kg(-1) x min(-1)) euglycemic hyperinsulinemic clamp combined with indirect calorimetry, we studied the effects of a LPD (0.3 g x kg(-1) x day(-1), supplemented with essential amino acids and ketoanalogs) in six patients suffering from chronic renal failure. After three months of diet, no significant change was observed concerning glomerular filtration rate, body wt, or arterial pH. In the postabsorptive state, plasma glucose and insulin levels were significantly lower, and energy production rose from 15.72 +/- 0.48 to 17.16 +/- 0.67 Cal x kg(-1) x min(-1) (P < 0.05). Insulin-stimulated glucose oxidation (2.36 +/- 0.29 vs. 3.37 +/- 0.35 mg x kg(-1) x min(-1); P < 0.05 at first clamp step) and nonoxidative disposal (P < 0.05 at both clamp steps) increased after LPD. This confirms that LPD ameliorates insulin sensitivity in CRF, even for low plasma insulin concentrations. Since energy production rate is increased by LPD, the caloric intake should be increased when protein intake is restricted.
Adult↗
A low-protein diet improves insulin sensitivity of endogenous glucose production in predialytic uremic patients.
A low-protein, low-phosphorus diet (LPD) has been shown to improve insulin sensitivity in uremic patients; however, this improvement has not been studied at low physiologic concentrations of plasma insulin, and the metabolic pathways concerned with this improvement have not been located. We used the glucose clamp technique at a low (0.25 mU.kg-1.min-1) level of hyperinsulinemia associated with the infusion of D[6,6-2H2] glucose to assess the insulin sensitivity of endogenous glucose production (EGP). Eight nondialyzed uremic patients were studied before and after 3 mo on an LPD providing 0.3 g/kg protein, 5-7 mg P/kg, and 146 kJ/kg (67% of energy as carbohydrates and 30% as lipids) per day, supplemented with ketoanalog amino acids. Postabsorptive plasma glucose and insulin declined after 3 mo of the diet (plasma glucose: 5.0 +/- 0.1 mmol/L before compared with 4.7 +/- 0.1 mmol/L after the LPD, P < 0.05; plasma insulin: 82.4 +/- 20.7 pmol/L before compared with 48.8 +/- 6.0 pmol/L after, P < 0.05). Postabsorptive glucose turnover rates did not change with the diet (2.06 +/- 0.14 mg.kg-1.min-1 before compared with 2.11 +/- 0.17 mg.kg-1.min-1 after LPD; NS). The insulin metabolic clearance rate was enhanced after the diet, so a lower level of hyperinsulinemia was obtained during the clamp (168.8 +/- 28.1 pmol/L before compared with 115.2 +/- 14.7 pmol/L after; P < 0.05). However, EGP was more easily inhibited after the diet (0.90 +/- 0.31 mg.kg-1.min-1 before compared with 0.30 +/- 0.17 mg.kg-1.min-1 after; P < 0.05), providing evidence of an improved insulin sensitivity of this parameter. This beneficial influence takes place at a physiologic level of hyperinsulinemia, and it probably plays an important role in the better glucose tolerance that has been reported in uremic patients on an LPD. An abnormal insulin sensitivity of EGP may participate in the disturbances of glucose metabolism in chronic renal failure.
Adult↗
Lipid-carbohydrate interactions in post-absorptive non-insulin-dependent diabetic patients.
Substrate competition is an important mechanism of insulin resistance, although its role in the post-absorptive hyperglycemia of NIDDM is not clear: lipid infusion does not raise plasma glucose levels in normal subjects, and total lipid oxidation, the elevation of which is a hallmark of disrupted carbohydrate metabolism, is normal in non-insulin-dependent diabetes mellitus (NIDDM). To examine further these two arguments against the involvement of lipid-carbohydrate interactions in the hyperglycemia of NIDDM, we compared the effect of a 3-hour lipid infusion ('Ivélip') on post-absorptive blood glucose levels, plasma lipids and respiratory exchanges in 15 patients with NIDDM, with that of an infusion of saline in 15 other patients with similar metabolic profiles. The lipid infusion significantly slowed the natural post-absorptive decline in blood glucose levels (saline -0.47 +/- 0.14 and Ivélip -0.10 +/- 0.12 mmol.l-1.h-1, p < 0.05), with marked interindividual differences. Substrate oxidation rates were unchanged during saline infusion, and were immediately (within 30 min) and reciprocally modified by the lipid infusion (lipid oxidation enhanced: 0.90 +/- 0.14 to 1.06 +/- 0.13 mg.kg-1.min-1 at time 30 min, p < 0.05; glucose oxidation inhibited: 1.27 +/- 0.19 to 0.87 +/- 0.18, p < 0.05), but this was not correlated with the alteration in blood glucose levels. In contrast, the increase in plasma lipids was continuous, and positively correlated with the change in blood glucose levels (r = 0.58, p < 0.05 for change of plasma free fatty acids; r = 0.55, p < 0.05 for change of plasma triglycerides, TGs). In line with the Randle mechanism, the lipid infusion affected oxidation rates, but another mechanism, depending on intravascular lipolysis of the infused TGs, was thought to occur in certain individuals whose blood glucose levels rose during the infusion.
Blood Glucose↗
Short-term insulin therapy and normoglycemia. Effects on erythrocyte lipid peroxidation in NIDDM patients.
OBJECTIVE: To evaluate erythrocyte lipid peroxidation (LPO) before and after an adaptive short-term insulin therapy in NIDDM patients who were chronically hyperglycemic. RESEARCH DESIGN AND METHODS: Twenty-six patients with NIDDM (mean HbA1c, 11.28%) aged 53.04 +/- 2.03 years were submitted for 3 days to constant intravenous glucose and continuous insulin perfusion at an adaptable rate to maintain glycemia within the normal range. An evaluation of LPO at baseline and after euglycemic insulin therapy was determined by erythrocyte free and total malondialdehyde (MDA) levels, polyunsaturated fatty acid (PUFA) percentage, vitamin E and glutathione content, and the following antioxidant enzymatic activity determinations: glutathione peroxidase (GPX), superoxide dismutase (SOD) and catalase (CAT). Fasting serum glucose, HbA1c, triglycerides, cholesterol, and HDL cholesterol levels were also determined at these time points. RESULTS: At baseline, erythrocyte free and total MDA were significantly higher in NIDDM patients than in control subjects (11.14 +/- 0.80 vs. 1.74 +/- 0.11 nmol/g Hb [P < 0.0001] for free MDA; 18.04 +/- 1.79 vs. 7.85 +/- 0.55 nmol/g Hb [P < 0.0001] for total MDA). PUFAs, particularly C20:4 and C22:5, were increased (14.69 +/- 0.34 vs. 12.03 +/- 0.31 and 2.31 +/- 0.04 vs. 1.71 +/- 0.03% of total fatty acids, respectively). Vitamin E and glutathione were reduced significantly (6.16 +/- 0.61 vs. 14.84 +/- 0.64 nmol/g Hb and 0.42 +/- 0.04 vs. 0.97 +/- 0.06 mmol/l, respectively). No difference was observed for the enzymatic activities. After euglycemic insulin therapy, triglycerides significantly decreased compared with baseline concentrations (1.55 +/- 0.13 vs. 2.42 +/- 0.22 mmol/l; P < 0.001), whereas other lipidic parameters were unchanged. Free MDA significantly decreased (8.60 +/- 0.76 vs. 11.14 +/- 0.80 nmol/g Hb [P < 0.01]), while vitamin E increased (7.93 +/- 0.73 vs. 6.16 +/- 0.61 nmol/g Hb [P < 0.05]). No difference was observed for PUFAs, glutathione, or total MDA. CONCLUSIONS: The observed erythrocyte LPO in NIDDM decreased after a short-term adaptive insulin therapy. This decrease could be principally attributed to the normalized glycemia that reduces reactive oxygen species (ROS) production, which in turn may explain the increase in erythrocyte membrane vitamin E and the decrease in MDA. This study shows the value of a euglycemic environment in NIDDM to reduce LPO and, at long range, to minimize clinical diabetes complications.
Adult↗
Acute painful diabetic neuropathy: two patients with recent insulin-dependent diabetes mellitus.
Two young men developed an acute painful peripheral neuropathy a few weeks after being diagnosed to suffer from an insulin-dependent diabetes mellitus. In both cases, peripheral nerve biopsy exhibited a few features of acute axonal degeneration. Additionally, in the first case there was a lymphocytic infiltrate around an endoneurial capillary, and in the second case there were several mast cells in the endoneurium of every fascicle examined. A few months later, the acute pain had disappeared in both cases. Only a few cases of acute painful diabetic neuropathy have been reported so far. A vascular origin seems unlikely and metabolic disorders are probably due to a contemporary severe weight loss. An auto-immune mechanism is an alternative explanation.
Acute Disease↗
Changes in phospholipid composition of blood cell membranes (erythrocyte, platelet, and polymorphonuclear) in different types of diabetes--clinical and biological correlations.
A variety of disorders of erythrocyte, platelet, and polymorphonuclear leukocyte (PMN) functions have been described in diabetes. The phospholipid composition of erythrocyte, platelet, and PMN membranes from controls and from type I and II diabetics was investigated in this study. Phospholipids were determined by densitometry using the molybdenum blue reagent. In diabetics, the relative abundance of phosphatidylethanolamine (PE) increased in all cell types studied, whereas those of sphingomyelin (Sph) and phosphatidylcholine (PC) were decreased in platelets and PMN. The percentage of phosphatidylserine (PS) was reduced in erythrocytes but increased in platelets. The level of Sph in PMN was significantly lower in type I than in type II diabetics. Moreover, the longer the duration of diabetes and the poorer the metabolic control, the greater the decrease in Sph. Rheological parameters, which reflect the behavior of red blood cells (RBC), were correlated with the alteration in PE/PS ratio in these cells.
Adult↗
Measurement of post-absorptive glucose kinetics in non-insulin-dependent diabetic patients: methodological aspects.
Post-absorptive glucose metabolism was studied in non-insulin-dependent diabetes mellitus (NIDDM) patients and normal subjects using dideuterated glucose as tracer. From the progressive fall in blood glucose levels and the increase in isotopic enrichment, the post-absorptive situation could not be regarded as a steady state for glucose metabolism, and non-steady-state approximations had therefore to be applied. However, this did not alter significantly the results in the 10 NIDDM patients studied. Significantly higher values of endogenous glucose production (EGP) were obtained (178 center dot 1 +/- 24 center dot 0 mg m-2 min-1 vs. 80 center dot 2 +/- 14 center dot 4; P < 0 center dot 01) if the tracer priming dose was not adapted to the degree of hyperglycaemia. Valid measurements could be made after only 1 h isotopic equilibration time if an appropriately matched priming dose was employed. Methodologically acceptable values for EGP in the 10 NIDDM patients did not differ significantly from those of 10 normal control subjects (80 center dot 2 +/- 14 center dot 4 mg m-2 min-1 vs. 85 center dot 6 +/- 3 center dot 9; not significant). The post-absorptive hyperglycaemia in these patients was assumed to stem essentially from a defect in peripheral glucose uptake.
Absorption↗
Recurrent aseptic purulent meningitis in a patient with relapsing polychondritis.
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Aged↗
[Hypoxemic pneumopathy in infectious mononucleosis in a 72-year-old man].
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Age Factors↗
Primary coinfection with human immunodeficiency virus and cytomegalovirus presenting as acute rhabdomyolysis.
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Acquired Immunodeficiency Syndrome↗
Extra-pancreatic manifestations in diabetes secondary to mitochondrial DNA point mutation within the tRNALeu(UUR) gene.
OBJECTIVE: A point mutation in the mitochondrial genome has been identified as a cause of diabetes and deafness. We report two pedigrees with and A-to-G transition at nucleotide 3243 of mtDNA within the tRNALeu(UUR) gene and focus our investigations on other localizations of the anomaly, particularly muscle and retina. RESEARCH DESIGN AND METHODS: Muscular localization has been studied in probands by invasive and noninvasive methods, including muscle biopsy (evaluation of the proportion of mutated mtDNA in comparison to blood cells, measurement of respiratory chain complex activities and histological and histochemical aspects) and 31P-nuclear magnetic resonance (NMR) spectroscopy. Ophthalmic and angiographic examination of retina, electroretinography, and visual evoked potentials were performed in five subjects. RESULTS: This mutation, previously described in patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), was expressed more abundantly in muscle than in nucleated blood cells. This low expression in blood cells could hamper the diagnosis for some patients. In addition, despite poor clinical expression, muscle was found to be highly affected. Ragged red fibers and dystrophic mitochondria were observed in muscle biopsy. Histochemical assays showed decreased activity of respiratory chain complexes, and 31P-NMR in vivo data further confirmed the defect of muscle oxidative processes. Exercise-induced lactate production was increased. Finally, in both families, an atypical "salt and pepper" pigmentary retinopathy was observed without consequences on visual acuity. CONCLUSIONS: In diabetes secondary to 3243 mtDNA mutation, infraclinical muscular and ocular lesions are frequent. These two locations of the disease, which are easily investigated by simple methods, can help in the diagnosis of this new type of diabetes.
Adult↗
[Endogenous production and peripheral utilization of glucose in patients with insulinoma].
Endogenous glucose production (EGP), glucose clearance and insulin sensitivity were measured in 5 subjects with insulinoma before and 3 to 6 months after surgical resection of the tumour. Endogenous glucose production and glucose clearance were evaluated by infusion of [6,6 D2] glucose, and insulin sensitivity was determined by a euglycaemic hyperinsulinaemic glucose clamp. The patients served as their own controls. The postabsorption blood glucose level was low before treatment (0.51 +/- 0.01 g/l) and EGP was 1.86 +/- 0.10 mg kg-1 min-1 (normal value: 2.2 to 2.6 mg kg-1 min-1), whereas the insulin level was relatively high (16.4 +/- 1.6 mU/l). After surgical resection of the insulinoma, the blood glucose level rose to 0.94 +/- 0.02 g/l and EGP to 2.33 +/- 0.04 mg kg-1 min-1, whereas the insulin level fell to 6.4 +/- 0.5 mU/l. Glucose metabolic clearance in the fasting state was 3.68 +2- 0.21 mg kg-1 min-1 before and 2.46 +/- 0.09 (n = 2.44 to 3.46 ml kg-1 min-1) after surgery. Clamp dose-response curves were shifted to the left and insulin sensitivity was improved after surgery. These data suggest that chronic hyperinsulinaemia is associated with inhibition of endogenous glucose production, a rise in basal glucose clearance and a state of insulin insensitivity during the clamp.
Adult↗
Effect of lipid infusion on postabsorptive glucose metabolism in non-insulin-dependent diabetic patients.
The effect of a lipid infusion on postabsorptive glucose metabolism was investigated in non-insulin-dependent diabetes mellitus (NIDDM) patients. During a basal period, plasma free fatty acids (FFA) and triglycerides, postabsorptive glycemia and insulinemia, and glucose turnover and metabolic clearance rates (MCRs) were measured in 10 NIDDM patients. After the basal measurement, five patients received a lipid infusion, and the others received saline. Lipid infusion prevented the decrease in postabsorptive glycemia observed in the saline group (P < .01). The principal mechanism for this effect was a reduction in glucose MCR (30.8 +/- 5.7 v 47.2 +/- 3.4 mL/m2/min, P < .05), which was absent in control tests (50.4 +/- 8.1 v 47.9 +/- 4.7 mL/m2/min, NS). The absence of the compensatory insulin release observed in normal subjects may play a role in this response. The prolonged postabsorptive hyperglycemia induced by lipid infusion in NIDDM patients is further evidence for the detrimental effect of the lipid-carbohydrate interactions described by Randle.
Absorption↗
Serum fatty acid profiles in type I and type II diabetes: metabolic alterations of fatty acids of the main serum lipids.
Fatty acid profiles of various lipid fractions were determined in carefully selected insulin-dependent and non-insulin-dependent diabetics to assess relationships between serum fatty acid composition and type of diabetes. Clear-cut hypertriglyceridemia with slight hypercholesterolemia was found in both diabetic types. The decrease of lignoceric acid in sphingomyelin is the only alteration found in both types of diabetes. In the insulin-dependent diabetics, there were increases in levels of oleic acid and of alpha-linolenic acid in esterified cholesterol, and in levels of alpha-linolenic acid in the triglyceride fraction. In the non-insulin-dependent diabetics, there were increases in levels of oleic acid and total monounsaturated fatty acids in the triglyceride fraction and there was an increase in levels of saturated fatty acids and a decrease in levels of polyunsaturated acids in phosphatidylcholine; in sphingomyelin, dihomogamma-linoleic acid levels were enhanced. Arachidonic acid levels were normal in our patient population.
Adult↗
[Mucorales infection in diabetics].
Naso-orbito-cerebral mucormycosis is a fungal infection reported to occur especially in association with diabetes mellitus. Mucorales germinate in the nasal cavities and then colonize sinuses and the orbit. The diagnosis must be made before meningeal and cerebral impairement. The diagnosis is based on histologic and mucologic examination. Once the diagnosis is confirmed, treatment required high and prolonged dose of intravenous Amphotericine B, otherwise the evolution is fatal.
Adult↗
[Clinical, biological and developmental aspects of cytomegalovirus infection in immunocompetent patients: apropos of 34 hospitalized patients].
We reviewed the thirty cases of cytomegalovirus infections with occurred in previously healthy patients, hospitalised for fever from 1981 to 1992. Pregnant women, transplant recipients, HIV infected persons and all immunocompromised subjects were excluded. We observed 34 cases (18 women, 16 men) whose mean age was 34 years (17 to 79). Fever appeared progressively (73%), persisted more than 15 days (87%) and was well tolerated. The main functional symptoms were headaches, myalgia (53%), profuse sweat (50%), abdominal pain, diarrhea, recent loss of weight, dry cough (51%). Splenomegaly was present in 24% of the cases. Chest X ray was always normal. Differential blood count was always inverse and an authentic mononucleosis syndrome was present in 91%: it appeared mainly 13 days after onset of symptoms. Hepatic abnormalities were nearly constant, especially cytolytic (97%) (transaminases three or four times upper the normal limit) but also cholestatic (62%). Thrombopenia has been noticed once (48,000/mm3). Serological diagnosis was confirmed with Elisa test (anti CMV Ig M: 30 cases) or complement fixation test (seroconversion: one, significant increase of the titers: two). CMV viremia, studied in seven patients, was positive in three. Spontaneous or treated (NSAI in 30%) outcome was nearly always favourable (97%). Two patients presented severe complications: meningo encephalitis and spleen rupture. CMV infection in previously healthy patients has to be suspected, without waiting for the mononucleosis syndrome, in view of a prolonged, well tolerated febrile illness, without pharyngitis, associated with hyperlymphocytosis and mild cytolysis. A careful follow-up is needed to detect the rare but severe complications.
Adolescent↗