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Biomedical subjects

H Gin

Publications and source records attributed to H Gin.

At least 55 records · Page 3Linked to original sources
PubMed2000

Lipids, protein intake, and diabetic nephropathy.

Progressive impairment of kidney function is one of the major problems in diabetic patients. Control of glycaemia and blood pressure is the main strategy for preventing or slowing impairment in renal function in this condition. However, contributing factors such as hyperlipidaemia and high protein intake have now been identified, and their control can be regarded as a complementary measure. The role of lipid abnormalities and hypercholesterolaemia in the pathogenesis of glomerular injury has been demonstrated in animal models, and a link between hypercholesterolaemia and diabetic nephropathy has been established in humans. To date, few intervention studies in diabetic patients have shown a slower decline in renal function. Nonetheless, in every study in which follow-up was long enough, cholesterol lowering had a beneficial effect on renal function. Although hypercholesterolaemia may not be the cause of renal injury, it represents an aggravating factor. High serum cholesterol seems to have a similar action on glomerular mesangial cells and endothelial cells. This appears to be analogous to the process of atherosclerosis, as mesangial cells possess binding sites for LDL and oxidised LDL, help recruit macrophages and secrete proliferative factors. Protein intake is another factor that can influence renal deterioration. Two meta-analyses have confirmed the beneficial effect of a low-protein diet in diabetic nephropathy, showing no adverse effects on the glycaemic control. Protein intake even seems to enhance the sensitivity of tissues and liver to insulin. Thus, there appear to be no contraindications to such diets in well-controlled diabetic patients. In short, although glycaemic and blood pressure control are still the main lines of treatment for diabetic patients, lowering blood cholesterol and restricting protein intake represent complementary measures that can help slow renal impairment.

Anticholesteremic Agents↗
PubMed2000

[Physiopathology of postprandial hyperglycemia].

Several factors are determinant for postprandial blood glucose. Knowing and analysing these factors will help to optimize diabetes management. First, meal introduces the concept of food glycemic index. Blood glucose peak following a meal is modulated by gut hormones incretin effect, essentially GIP and GLP1. At the hepatic level, 30% of absorbed glucose is extracted by the liver which reduces its endogenous production in parallel. A reduction in hepatic glucose production blockade--through an excess in glucagon or free fatty acids in portal flow--will result in postprandial hyperglycemia. Finally, insulin secretion pattern is less influent than the hepatic insulin resistant state itself in determining this hyperglycemia.

Blood Glucose↗
PubMed2000

Post-prandial hyperglycemia. post-prandial hyperglycemia and diabetes.

Post-prandial hyperglycemia (PPHG) is an independent risk factor for the development of macrovascular complications. It is now recognized that normalizing post-prandial blood glucose is more difficult than normalizing fasting glucose. Many factors affect the post-prandial blood glucose excursion. The glycemic index of the meal depends on the nature of the ingested food and starch composition. Gastric emptying is influenced by various factors including gut hormones such as GIP and GLP1, which potentiate insulin secretion, especially in its acute first phase, now referred to as an incretin effect. They also modulate glucagon secretion. Post-prandial hyperglycemia is limited by uptake of glucose by the liver and by inhibition of endogenous glucose production in this organ. In healthy controls, hepatic glucose production is halved after a meal, whereas in glucose-intolerant individuals and type 2 diabetics this inhibition is impaired (20-30% versus 50%). The persistence of endogenous glucose production during the post-prandial phase appears to be the main culprit in the PPHG. This reduced decrease in endogenous glucose in glucose intolerant and type 2 diabetic patients depends not only on the first acute phase of insulin secretion, but above all on the non-suppressed glucagon level during the post-prandial phase. Glucagon levels fall in healthy control subjects during the post-prandial phase. Although peripheral glucose uptake by insulin-dependent tissues is altered in type 2 diabetic patients, it does not appear to be the major cause of the PPHG as there are patients with insulin resistance but without post-prandial hyperglycemia.

Animals↗
PubMed1999

Thermogenic effect of slight hyperglycemia during a lipid infusion.

Resistance to the glucoregulatory action of insulin is a common finding in obesity and may affect thermogenesis. In 13 healthy subjects, we studied the influence of acute insulin resistance induced by a lipid infusion on thermogenesis without any glucose load (n = 4) or during a euglycemic-hyperinsulinemic clamp (n = 5) and an oral glucose tolerance test (OGTT, n = 8). When substrates were not administered at the same time, the energy cost of storage was significantly (P < .05) lower for lipids (3.9%+/-0.9%) than for glucose (11.9%+/-0.5% during the clamp and 14.9%+/-4.0% during the OGTT, NS). The lipid infusion decreased glucose storage during the clamp (control, 3.99+/-0.40 mg x kg(-1) x min(-1); lipid infusion, 0.92+/-0.39; P < .05) but increased it during the OGTT (control, 1.76+/-0.22 mg x kg(-1) x min(-1); lipid infusion, 2.94+/-0.27; P < .05). Infused lipids were stored more (clamp, 3.31+/-0.16; OGTT, 2.65+/-0.11 mg x kg(-1) x min(-1); P < .01) and oxidized less (clamp, 0.64+/-0.21; OGTT, 1.02+/-0.09 mg x kg(-1) x min(-1); P < .05) during the clamp than during the OGTT. When lipids were infused, the energy cost of substrate storage was lower during the clamp versus the OGTT (clamp, 3.2%+/-0.8%; OGTT, 7.3%+/-1.0%; P < .05). This effect was attributed to a lipid-induced impairment of glucose tolerance, which overcomes the inhibitory effect of lipid infusion on glucose storage observed in euglycemia. A slight elevation of plasma glucose in response to a lipid infusion impairs thermogenesis by redirecting the storage of substrates from lipids to glucose, which has a higher energy cost.

Adult↗
PubMed1999

Effects of red wine, tannic acid, or ethanol on glucose tolerance in non-insulin-dependent diabetic patients and on starch digestibility in vitro.

This study examines the effect of moderate intake of red wine, tannic acid, or ethanol during a meal in type 2 diabetic patients and the influence of tannic acid on the digestibility of starch by alpha-amylase. Thirty non-insulin-dependent diabetes mellitus (NIDDM) patients aged 53 +/- 6 years were studied (in vivo study) 10 of whom received red wine (200 mL), 10 tannic acid (150 mg), and 10 ethanol (16 g) with their midday meal (600 calories, 65 g carbohydrate, 20 g lipid, and 34 g protein). All patients were tested on two occasions (water or placebo v wine, alcohol, or tannic acid). The influence of tannic acid (0.25, 0.5, and 1 mg) on the digestibility of starch (100 mg) by alpha-amylase (100 U) was tested in vitro by sequential incubation at 37 degrees C (in vitro study). The maximum glucose excursion after lunch was 2.6 +/- 0.8 mmol/L at 90 minutes (T90) for water and 1.8 +/- 0.9 mmol/L at T90 for red wine taken with the meal. The values at T60 and T90 were significant (P < .01). Comparable results were obtained with tannic acid alone (nonalcoholic component of wine): the maximum glucose excursion after lunch was 2.76 +/- 0.9 mmol/L at T120 for placebo and 1.97 +/- 0.9 mmol/L at T90 for tannic acid (P < .01); no difference in glucose and insulin excursion was observed between water and ethanol. No interaction between tannic acid and starch was observed in the in vitro experiments, although after preincubation of alpha-amylase with tannic acid, digestion was slowed in a dose-dependent manner (6.1 +/- 1.1 minutes for 0.25 mg tannic acid and 13.1 +/- 1.59 minutes for 1 mg tannic acid). Drinking red wine with a meal did not increase blood glucose in NIDDM patients, and led to a slight decrease in some instances. The effect appeared to be mediated by the nonalcoholic compounds in wine such as tannic acid. Ethanol itself had no effect on plasma glucose or insulin levels.

Blood Glucose↗
PubMed1999

Prevalence of macular pattern dystrophy in maternally inherited diabetes and deafness. GEDIAM Group.

OBJECTIVE: To evaluate the prevalence of macular pattern dystrophy (MPD) in maternally inherited diabetes and deafness (MIDD), a new subtype of diabetes mellitus that cosegregates with a mutation of mitochondrial DNA (i.e., the substitution of guanine for adenine at position 3243 of leucine transfer RNA) and to report the clinical characteristics of MPD. DESIGN: Prospective cohort study. PARTICIPANTS: Forty-six patients from 29 families with an adenine-to-guanine mutation of mitochondrial DNA were recruited from a French collaborative multicenter study. Thirty-five patients had MIDD, 8 were asymptomatic children of MIDD patients, and 3 had MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes). The 33 MIDD patients with diabetes were matched for diabetes duration and gender with 33 patients with "common" type-2 diabetes to compare the prevalence of diabetic retinopathy (DR) in both series. METHODS: All patients had a full ophthalmologic examination and fundus photographs. MAIN OUTCOME MEASURES: The presence and severity of MPD and DR were assessed in each patient. RESULTS: Thirty MIDD patients (85.7%) of 35 exhibited bilateral MPD characterized by linear pigmentation surrounding the macula and optic disc. In 24 of these 30 patients, visual acuity was 20/25 or more in both eyes. The prevalence of DR was 6% in MIDD patients with diabetes versus 15% for patients with common type-2 diabetes (a difference that was not significant, P = 0.23). The fundus of each of the eight asymptomatic children was normal. MPD was present in one of the three cases of MELAS. CONCLUSION: The prevalence of MPD in MIDD is high. Its detection may be helpful for the diagnosis of this new subtype of diabetes, for which specific treatments may be proposed.

Adult↗
PubMed1999

13C nuclear magnetic resonance study of glycogen resynthesis in muscle after glycogen-depleting exercise in healthy men receiving an infusion of lipid emulsion.

In healthy individuals, glycogen recovery after a strong depletion is known to be rapid and insulin independent during the initial phase, and subsequently, slow and insulin dependent. Free fatty acids (FFAs) as a putative source of insulin resistance (IR) could thus impair glycogen recovery during the second period. Using in vivo 13C nuclear magnetic resonance (NMR), we studied the effect of long-chain triglyceride emulsion on gastrocnemius glycogen resynthesis during a 3-h recovery period after 90 min of moderate exercise consisting of plantar flexion on overnight-fasted healthy men (n = 8). In separate experiments, each subject was infused with 10% Ivelip (0.015 ml x kg(-1) x min(-1)) or 10% glycerol (0.13 mg x kg(-1) x min(-1)). NMR spectra were acquired before and at the end of the exercise and during the recovery period. Whole-body glucose and lipid oxidation rates (indirect calorimetry), plasma insulin, C-peptide, glucose, lactate, beta-hydroxybutyrate, triglycerides, and FFAs were determined. Glycogen consumption was 47.6 +/- 4.5% (glycerol) and 49.7 +/- 4.8% (Ivelip) of the initial glycogen. An acquired IR in the Ivelip group was significant at the onset of the recovery period by homeostasis model assessment (P = 0.002). Glycogen resynthesis in the glycerol group appeared faster during the 1st h than during the subsequent 2nd h of the postexercise period. The glycogen resynthesis level was significantly lower in the Ivelip group than in the glycerol group during the recovery period (P = 0.04 during the 1st h and P = 0.001 during the next 2 h). During the recovery, plasma lactate and whole-body oxidation rates were similar in the two groups, whereas glycemia was significantly higher in the Ivelip group. A decreased cellular uptake of glucose as a substrate for glycogenosynthesis, rather than a competition between oxidation of carbohydrate and FFA, is discussed.

Adult↗
PubMed1999

Determination of glucose in dried serum samples by Fourier-transform infrared spectroscopy.

BACKGROUND: Practical improvements are needed to allow measurement of glucose concentrations by Fourier- transform infrared (FT-IR) spectroscopy. We developed a new method that allows determination of the glucose concentration in dried sera. METHODS: We studied 32 serum samples after fourfold dilution and desiccation before FT-IR analyses on a spectrometer operated at a resolution of 2.0 cm(-1). We integrated all spectral windows at the surface of the spectrum in the C--O region. For comparison, glucose was measured in the sera by a glucose oxidase method. RESULTS: One peak within the spectrum was most specific for glucose (997-1062 cm(-1)). Its surface integration showed a strong relationship with reference data (r = 0.998; P <0.001). FT-IR analyses of five glucose solutions were performed to determine its specific absorption at the same peak. In this way, glucose concentrations in serum spectra could be measured. For the first time while using FT-IR spectroscopy, no manipulation of spectra nor use of internal standard was necessary to obtain results in high accordance with glucose concentration measured by a conventional (glucose-oxidase) method (S(y|x) = 0.25 mmol/L; r = 0. 998). CONCLUSIONS: FT-IR spectroscopy appears to be an easy and accurate method to determine glucose concentration and could be widely used to simultaneously identify and quantify several metabolites in biological fluids or tissues.

Adult↗
PubMed1999

[Insulin resistance: therapeutic approaches].

NIDDM is characterized by a decrease in insulin sensitivity of the liver, the muscles and adipocytes. Diet, exercise and control of excess body weight are the first step of the treatment; they are even able to prevent NIDDM. In this paper the drugs that may improve insulin sensitivity are described with their different specific action on liver, muscles, or adipocytes. Drugs from the thiazolidinedione class act by enhancing the sensitivity to insulin of adipose tissue; they are high-affinity ligands for peroxisome proliferator-activated receptor gamma 2 (PPAR gamma 2 being the predominant form expressed in adipocytes) Hepatotoxicity and weight gain are sides effects of thiazolidinedione. Acipimox (a nicotinic acid analogue) is a NEFA lowering drug that suppress lipolysis, but after a few days of utilisation there is a compensatory free fatty acid rise. Recent data on Metformin action on hepatic insulin sensitivity are discussed and combination with Troglitazone is presented. Vanadyl sulfate may also improve insulin sensitivity but there is no long term human studies.

Combined Modality Therapy↗
PubMed1999

Composition of insulin-induced body weight gain in diabetic patients: a bio-impedance study.

Although insulin is a well-known cause of body weight gain, it is not clear whether it is due to the accumulation of fat or lean mass. We performed a 3 months Body-Impedance Analysis follow-up in 72 diabetic patients in a wide range of insulin indications: insulin introduction in young inaugural type 1 diabetics (n = 12), late-onset type 1 (n = 12), type 2 affected by intercurrent diseases (n = 12) or microangiopathic complications (n = 12), type 2 with failure of oral antidiabetic agents (n = 12), and insulin withdrawal in type 2 (n = 12). In type 1 patients, insulin led to the most important weight gain, but it was fat-free, with a major benefit on HbA1C. Type 2 patients affected by intercurrent diseases or microangiopathic complications had a mild, also fat-free weight gain, with a clear benefit on HbA1C. In type 2 patients with failure of oral agents, HbA1C declined less, weight gain was intermedia, but predominantly fat, mirrored by a predominant fat loss in type 2 patients whose insulin was stopped (without significant change in HbA1C). Both fat and lean mass contributed to insulin-induced body weight gain, but a significant negative relationship existed between their respective evolution in our patients (r = -0.23, p < 0.05 by linear regression analysis between delta fat mass and delta lean mass). Insulin-induced body weight gain is not univocal: insulin restaures or protects lean mass in its less controversial indications, whereas it leads to fat accumulation in type 2 patients with isolated failure of oral agents.

Adult↗
PubMed1998

Electrophysiological monitoring in clinical trials. Roche Neuropathy Study Group.

Electrophysiological testing remains an important efficacy parameter in clinical neuropathy trials. The quality of nerve conduction studies in reported trials varies greatly, and may be responsible for negative results. We report the utilization of an expert core lab for electrophysiological testing. With the core lab, the variability of repeat testing is comparable to that of a single, excellent laboratory. Motor conduction velocities demonstrated a coefficient of variation of 3% and sensory conduction velocities 4% across 60 study sites. The distal motor evoked potential amplitudes varied by 13% at the ankle, and 10% at the wrist. The sensory potential amplitudes varied by 16% at the ankle, and 11% at the wrist in 60 sites. The overall monitoring rate in all submitted nerve conduction tracings was 36.6%. Our results show that an expert core lab can improve the electrophysiological quality of clinical trial data with the potential to show small changes in nerve conduction velocities and in both motor and sensory potential amplitudes.

Diabetic Neuropathies↗
PubMed1998

The place of electron spin resonance methods in the detection of oxidative stress in type 2 diabetes with poor glycemic control.

OBJECTIVE: Chronic production of reactive oxygen species (ROS) and/or deficiency in the antioxidant defense system are observed in non-insulin-dependent diabetes mellitus (NIDDM) patients. As an adjunct to the usual indirect parameters for evaluating oxidative stress, we assessed the feasibility of oxyradicals detection in venous blood by electron spin resonance spectroscopy (ESR). Detection of the ascorbate pool was also performed using the validated ESR analysis of the ascorbyl free radial (AFR)-dimethyl sulfoxide (DMSO) complex. METHODS AND RESULTS: Plasma lipoperoxidation was characterized by higher levels of total MDA (1.50 +/- 0.08 nmol/L), lower levels of GSH (0.54 +/- 0.02 mmol/L) and of vitamin A (2.13 +/- 0.52 mumol/L) in the NIDDM group than in the controls (0.75 +/- 0.05 nmol/L, 0.90 +/- 0.05 mmol/L, 3.52 +/- 1.04 mumol/L, respectively). Improvement of the ESR measurement of oxyradical adducts has been previously obtained by addition of a new sensitive nitrone (DEPMPO), which acts as a spin-trap. However, in our experiment the ESR signal-to-noise ratio was too low to detect significative oxyradicals adducts in total venous blood of NIDDM patients having a weak production of ROS. A significant difference (p < 0.002) was observed in DMSO/AFR index between controls (24.00 +/- 4.10 nmol/L) and NIDDM patients (7.28 +/- 2.36 nmol/L) suggesting ascorbate depletion related to the free radical production. CONCLUSION: The DMSO/AFR index could be an interesting additional marker of oxidative stress during a chronic production of ROS.

Adult↗
PubMed1998

Effects of low-protein diet on carbohydrate metabolism and energy expenditure.

Low-protein diets (LPD), which are prescribed for uremic patients to slow the progression of chronic renal failure, theoretically may exacerbate disorders of carbohydrate metabolism that are frequently observed in these patients because increased carbohydrate rations are required to maintain a sufficient caloric intake. No such exacerbation actually occurs. Glucose tolerance has been shown to improve after 3 months of a diet affording .3 g protein/kg body weight supplemented with essential amino acids and ketoanalogs with carbohydrates accounting for 67% of the total energy intake. Hyperinsulinemic euglycemic clamp studies show that this amelioration is linked with an increase in insulin sensitivity, which is also observed in uremic diabetic patients on this diet. The improvement in glucose tolerance involves the insulin sensitivity of endogenous glucose production, glucose oxidative disposal, and its nonoxidative disposal. Besides these effects, LPD increases the metabolic clearance rate of insulin and causes blood insulin levels to decrease. LPD's low acid load and phosphorus content, the reduced synthesis of uremic toxins derived from alimentary protein, or both may explain these effects, which are indirectly protective against atherosclerosis. However, the significant increase in resting energy production after 3 months on LPD justifies strict monitoring of nutritional status and caloric intake.

Basal Metabolism↗
PubMed1998

Mechanisms of glucose intolerance during triglyceride infusion.

Lipid infusions may affect glucose tolerance by effects on glucose production or utilization. We performed double-labeled oral glucose tolerance tests with and without a lipid infusion in eight normal subjects. During the lipid infusion, plasma glucose and insulin levels were higher, showing some insulin resistance. The increased glucose level was due to a higher total glucose appearance rate, partly reproducible by a control infusion of glycerol [saline 1,181 +/- 71 mg . kg-1 . 330 min-1 vs. lipid 1,388 +/- 100 (P < 0.05) vs. glycerol 1,276 +/- 126 (NS)]. The tracer-determined appearance rate of exogenous glucose was higher with lipid infusion but was probably overestimated because of higher 13C recycling into glucose. Residual systemic glucose production was increased but was reproducible by the glycerol infusion. Total glucose disposal was increased. This was observed despite a lower stimulation of total glucose oxidation as measured by indirect calorimetry, whereas oxidation of exogenous glucose was normal after correction for the lipid-induced modification of excretion rate of 13CO2. Accordingly, glucose nonoxidative disposal was increased. These moderate modifications of glucose metabolism (increased appearance, increased nonoxidative disposal, and lower total oxidation) have been reported in starvation-induced or spontaneously impaired glucose tolerance. Further impairment, especially decreased nonoxidative glucose disposal, seems to be required to produce non-insulin-dependent diabetes mellitus.

Blood Glucose↗
PubMed1998

Experience with the Biostator for diagnosis and assisted surgery of 21 insulinomas.

Surgical removal is the treatment of choice for insulinomas. Definitive biochemical diagnosis of organic hyperinsulinism has to be established before surgery. These tumors are sometimes undetected by preoperative imaging investigations and, in addition, surgical management may also be complicated by the absence of palpable tumors or the presence of multiple tumors. We report the value of the euglycemic clamp technique for diagnosis and surgical treatment in 21 patients with confirmed insulinomas. Data were compared with 12 controls, and nine patients were retested after surgery. During the euglycemic hyperinsulinic clamp, the mean C-peptide value was 3.6+/-2.2 ng/ml and it remained high (3.8+/-2.5 ng/ml), despite exogenous hyperinsulinemia (1762.7+/-233.2 microU/ml for the highest plateau). In contrast, the C-peptide concentration declined in 12 control patients (0.3+/-0.1 ng/ml, P < 0.001) and after successful surgery in nine retested patients (0.3+/-0.2 ng/ml, P < 0.01). During continuous glucose monitoring, successful removal of the insulin-secreting tumor was accompanied by an increase in plasma glucose concentrations and a loss of requirement for endogenous glucose within 36 min (range 28-43 min). The continuing requirement for glucose after the ablation of the tumor revealed the existence of additional and initially undetected tumors in four patients, among whom two had the multiple endocrine neoplasia type I (MEN I) syndrome. We conclude that the euglycemic hyperinsulinic clamp is a reliable and convenient diagnostic test for insulinoma, as it is both safe (no hypoglycemia) and relatively brief (3 x 90 min). Glucose monitoring and glucose clamping provide a reliable indicator of complete removal of insulin-hypersecreting tissue, especially in patients with occult or multiple tumors.

Adult↗
PubMed1998

Erythropoietin can deteriorate glucose control in uraemic non-insulin-dependent diabetic patients.

Two patients with non-insulin-dependent diabetes mellitus (NIDDM) and moderate chronic renal failure experienced a worsening of glycaemic control when recombinant human erythropoietin (r-HuEPO) was introduced, leading to insulin therapy. A 71-year-old woman with a 20-year history of NIDDM had presented histologically documented diabetic nephropathy for 2 years during which glucose control was stabilized by a diet and glibenclamide 10 mg. In the 6 months following introduction of r-HuEPO, hyperglycaemic symptoms developed, and HbA1C increased from 8.9% to 12.3%. During this period, no intercurrent events occurred, except epistaxis due to accelerated hypertension one month after r-HuEPO was started. A 62-year-old man had a 15-year history of NIDDM, with proliferative retinopathy, macroproteinuria and chronic renal failure for 4 years. The day after the first injection of r-HuEPO, capillary glucose level rose dramatically. In both of these cases, antihypertensive treatment was increased and insulin introduced. The role of r-HuEPO in hyperglycaemia was probable in the first case and highly probable in the second. Reports about the effects of r-HuEPO on glucose metabolism in uraemic patients are conflicting. Short- and long-term effects can differ, although long-term benefit is likely. The fact that our patients were not dialized may have been important. Clinicians should be aware that glucose control may deteriorate with r-HuEPO, requiring some uraemic NIDDM patients to undergo insulin therapy.

Aged↗