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H Gin

Publications and source records attributed to H Gin.

At least 37 records · Page 2Linked to original sources

Relationship between peroxisome proliferator-activated receptor gamma and retinoic acid receptor alpha gene expression in obese human adipose tissue.

OBJECTIVE: To investigate in human adipose tissue a possible relationship between per oxisome proliferator-activated receptor gamma (PPARgamma) and retinoic acid receptor alpha (RARalpha) gene expression, two genes involved in the control of adipocyte differentiation. SUBJECTS: Ten lean control women (age 31-60 y, body mass index (BMI) 18-24.7 kg/m(2)) and an obese group of 15 women (age 27-62 y, BMI 30-57.5 kg/m(2)), of whom 10 subjects were in weight-gain phase and five were in weight-loss phase. MEASUREMENTS: We assessed the relative PPARgamma and RARalpha mRNA levels in subcutaneous abdominal adipose tissue using a real-time PCR method. RESULTS: PPARgamma mRNA level were significantly increased (+91%; P<0.01) in obese women compared to lean control women. In the obese group, we observed a PPARgamma mRNA level 42% lower in weight-loss obese than in weight-gain obese subjects. We obtained a positive correlation (r=0.56; P<0.01) between PPARgamma mRNA level and the BMI of all subjects. Relative mRNA abundance level of RARalpha in subcutaneous adipose tissue of obese subjects is significantly lower than in control subjects (-56%, P<0.01), and a negative correlation was found between PPARgamma and RARalpha mRNA levels in subcutaneous adipose tissue of subjects study (r=-0.75; P<0.01). CONCLUSION: Our findings suggest that obesity is associated with an inverse relationship between PPARgamma and RARalpha expressions in human subcutaneous adipose tissue. Modulations of nuclear receptor profile could be an important event in the body's early adaptive mechanisms promoting adipose tissue plasticity and leading to the onset of obesity.

Adipose Tissue↗

Atrial fibrillation can cause major hyperglycemia.

We report the case of a 66 years old woman with a well controlled, insulin-treated, type 2 diabetes, who experienced a ten-fold increase of her daily insulin needs (from 21 to 215 U/day) after the onset of a symptomatic atrial fibrillation. Check-up for another cause of insulin resistance was negative, and insulin doses could be decreased to preceding values only after electric cardioversion. Symptomatic atrial fibrillation should be considered as a potential cause of hyperglycemia.

Aged↗

[Screening for peripheral neuropathy: which tools?].

Peripheral diabetic neuropathy is asymptomatic as other diabetic complications. However it can have potentially serious consequences such as the development of foot ulcerations and foot amputation. Early identification of high-risk diabetic patients is needed but one must keep in mind that peripheral neuropathy always begin at the extreme distality of the lower limbs and that it may be detected at the toe level and not at the ankle level; moreover, diabetic peripheral neuropathy can affect different type of fibers and different explorations are needed for an early diagnosis. There are different tools such as monofilament, tune fork, or vibration bioesthesiometer but each has its limits and must be used with caution for being valid; some are qualitative, others are quantitative. The early detection of the high-risk patient can focus the attention of the medical and nurse team on those patients which will benefit from self foot care.

Diabetic Neuropathies↗

Oral anti diabetic polychemotherapy in type 2 diabetes mellitus.

The therapeutic guidelines of the seventies for type 2 diabetic patients was a monotherapy which choice was based on the BMI of the patient and a bitherapy in case of a blood glucose increase. The pathophysiologic knowledge on type 2 diabetes has moved and the disease is nowadays more complex with a loss of the beta cell mass and an insulin resistance state of the liver, muscle and adipocyte tissue associated with a defect in gastro-intestinal hormones in the postprandial state. The pathophysiologic knowledge and the existence of new therapeutic agents led us to discuss oral antidiabetic polychemotherapy at the first drug prescription. This intuitive proposition has no evidence-based arguments with prospective long-term studies that would demonstrate the benefit of such a proposition. Moreover, if nowadays we can imagine a tritherapy proposition, progress in chemistry research will conduct to a quadri- and penta-therapy with expected difficulties in therapeutic compliance of the patient.

Administration, Oral↗

Comparison between monofilament, tuning fork and vibration perception tests for screening patients at risk of foot complication.

OBJECTIVE: To compare normal and pathologic values of three different tests for screening patients at risk of foot complications: mono-filament, tuning fork and vibration threshold perception (VTP). METHODS: Two hundred and fifty consecutive patients followed-up in a diabetic clinic were screened for sensitive polyneuropathy by three different tests in three different examinations in a blind design. The 10 g mono-filament, tuning fork and Horwell neuro-esthesiometer were applied to different sites on the patients' legs and feet. RESULTS: Thirty eight patients were identified having abnormal tests and being at risk of foot complications using the mono-filament test; 33 of them and 9 more (42 patients (33 + 9)) were identified using the tuning fork applied to the malleolus and eight more (50 patients (33 + 9 + 8)) when the tuning fork was applied to the big toe; twenty more patients (70 (33 + 9 + 8 + 20)) were identified as being at risk using the VTP at a cut-off of 25 V. CONCLUSION: The mono-filament test identified patient with the highest risk of foot complications, but 37 more patients were identified to be at risk from a VTP > 25 V. These patients were not detected using the mono-filament test. The VTP test provides numerical values that can help to follow the course of the risk for foot insensitivity by allowing the care team to grade the education and follow-up of the at-risk group.

Adolescent↗

Maternally inherited diabetes and deafness: a multicenter study.

BACKGROUND: Maternally inherited diabetes and deafness (MIDD), which is seen in 0.5% to 2.8% of patients with type 2 diabetes mellitus, is related to a point mutation at position 3243 of mitochondrial (mt) DNA. Its clinical description is incomplete. OBJECTIVE: To study the clinical presentation and complications of diabetes in patients with MIDD and to identify clinical characteristics that may help select diabetic patients for mtDNA mutation screening. DESIGN: Multicenter prospective descriptive study. SETTING: 16 French departments of internal medicine, diabetes and metabolic diseases, or both. PATIENTS: 54 patients with type 2 diabetes mellitus and the mtDNA 3243 mutation. MEASUREMENTS: Characteristics of diabetes, metabolic control (glycosylated hemoglobin level), complications of diabetes, and involvement of other organs. RESULTS: On average, patients with MIDD were young at diabetes onset and presented with a normal or low body mass index. None were obese. Seventy-three percent of probands had a maternal family history of diabetes. Diabetes was non-insulin-dependent at onset in 87% of patients; however, 46% of patients had non-insulin-dependent disease at onset but progressed to insulin therapy after a mean duration of approximately 10 years. Neurosensory hearing loss was present in almost all patients. Eighty-six percent of patients who received an ophthalmologic examination had macular pattern dystrophy (a specific retinal lesion). Forty-three percent of patients had myopathy, 15% had cardiomyopathy, and 18% (9 of 51) had neuropsychiatric symptoms. Although the prevalence of diabetic retinopathy was 8% among patients who received an ophthalmologic examination, lower than expected after a mean 12-year duration of diabetes, prevalence of kidney disease was 28%. This suggests that a specific renal involvement was the result of mitochondrial disease. CONCLUSIONS: Maternally inherited diabetes and deafness has a specific clinical profile that may help identify diabetic patients for mtDNA testing.

Adolescent↗

[Clinical diagnosis of overtraining using blood tests: current knowledge].

PURPOSE: Overtraining results from an imbalance between training load-induced fatigue and organism's recovery abilities. Its etiology is complex and to date there is no useful clinical diagnostic tool. The purpose of this review is to discuss the blood chemistry parameters potentially useful for diagnosing overtraining in athletes. CURRENT KNOWLEDGE AND KEY POINTS: Chronic alterations of the myocyte structure may cause high plasma concentration increases of myoglobin, troponin I and creatine kinase enzyme, resulting in chemical and/or mechanical aggression. Monitoring reactive oxygen species' activity appears to be a good tool for evaluation of the metabolic stress level experienced by skeletal muscles. In energetic metabolism, a succession of chronic glycogen depletions might change the use of amino acids and lipids, inducing transient but severe hypoglycemia during exercise. A higher oxidation of circulating glutamine might cause immunosuppression (lower reactivity to inflammations and cellular traumatisms), inhibiting alarm signals during acute training. A higher branched-chain amino acid oxidation might favor free tryptophan's entry into the cerebral area, enhancing serotonin synthesis. As a consequence, asthenia and a loss of sensitivity to muscular and tendon traumatism might appear. Exercise anemia might also be a worsening factor of the physiological situation of the tired athlete, inducing predisposition to overtraining by the lower inflammation reactivity of depleted hepatic and muscular proteins. FUTURE PROSPECTS AND PROJECTS: Early diagnosis of overtraining diagnosis may be established only from a battery of analyses, which should include the whole of the potential parameters. These remain unpredictable and do not allow systematic determination of new cases. Only a longitudinal study of the physiological situation appears to allow the necessary conditions for detecting overtraining in the early stages of its process for each subject.

Biomarkers↗

CPAP treatment does not affect glucose-insulin metabolism in sleep apneic patients.

Objective: We investigated glucose metabolism and insulin resistance in non-obese and moderately overweight sleep apnea patients, as well as their response to nasal CPAP treatment.Methods: A group of subjects with glucose intolerance was screened for sleep disordered breathing by clinical interview and ambulatory recordings. Ten subjects were found to have untreated sleep apnea and were asked to participate in further investigation. This included nocturnal polysomnography, oral glucose tolerance test and indirect calorimetry. Subjects then had calibration of nasal CPAP with polysomnography. Two months after start of treatment, all subjects were restudied as at baseline. In parallel, six obstructive sleep apnea syndrome (OSAS) subjects, diagnosed through the sleep clinic, were matched for gender, age and oxygen desaturation index with the other group, and had a euglycemic hyperinsulinemic clamp at baseline and after 2 months of nasal CPAP.Results: The first ten patients showed no change in total glucose oxidation, glucose oxidation by weight or by fat free mass, or insulin energetic expenditure, despite nocturnal usage of nasal CPAP. Similarly, when comparing baseline to the treatment at 2 months, the six OSAS patients had no change in mean glycemia, insulin, C peptide and hemoglobin (Hgb) A1C measurements. No difference in the amount of glucose infused during the duration of the clamp was noted either.Conclusion: Our data do not support the existence of a significant relationship between glucose and insulin metabolism and obstructive sleep apnea. Obesity, when present, is the important variable.

Journal Article↗

Energy expenditure following oral glucose load in ten uremic patients before and after three months on a ketoacid-supplemented very-low-protein diet.

We have previously shown that a ketoacid-supplemented very-low-protein diet (KSVLPD), which has been proposed to slow down the rate of progression of chronic renal failure (CRF), improves tissue insulin sensitivity and decreases hyperinsulinemia in predialytic uremic patients. However, this diet may interfere with nutritional status. The aim of this study was to study basal energy expenditure (EE) and EE after an oral glucose load in patients with CRF before and during a KSVLPD (0.3 cal x kg wt(-1) x d(-1) supplemented with aminoacid and ketoanalogs) using oral glucose loading in combination with indirect calorimetry. We also monitored body weight and analyzed body composition by dual-energy x-ray (DEXA) during KSVLPD. In the third month of KSVLPD, no significant change in total body weight was observed, but DEXA showed a decrease in lean tissue mass (LTM; 46.2 +/- 3.6 kg before v 44 +/- 3.4 kg in the third month; P <.01) and an increase in body fat mass (20.1 +/- 2.4 kg before v 21.3 +/- 2.4 kg on KSVLPD; P <.05). Postabsorptive plasma glucose level was significantly lower, and glucose oxidation and energy expenditure per LTM were significantly increased (EE, 20 +/- 0.8 cal x kg LTM(-1) x min(-1) before diet v 21.9 +/- 1.1 cal x kg LTM(-1) x min(-1) after 3 months on KSVLPD; P <.01). Plasma glucose and serum insulin levels were significantly lower after glucose loading, and glucose oxidation increased. EE values were significantly higher after the oral glucose load, and cumulative EE after oral load increased from 20.7 +/- 0.7 cal x kg LTM(-1) x min(-1) before the diet to 22.9 +/- 1.1 cal x kg LTM(-1) x min(-1) in the third month of KSVLPD; P <.001). Glucose oxidation was higher and cumulative glucose storage was decreased after diet (29.6 +/- 4.2 g v 20.9 +/- 3.4 g on KSVLPD; P <.01). We conclude that KSVLPD increases EE in the postabsorptive state and after an oral glucose load with an adaptation of lean tissue mass in the third month of the diet. Therefore, during KSVLPD, strict monitoring of dietetic management is necessary to maintain energy requirements at high levels appropriate to the new EE.

Administration, Oral↗

Differentiation of populations with different physiologic profiles by plasma Fourier-transform infrared spectra classification.

The pathologic condition of a patient presenting a metabolic disease can change rapidly, and a variety of pathologic conditions are possible. Plasma Fourier-transform infrared (FT-IR) spectra were used to differentiate patients with type 1 diabetes, healthy subjects, and endurance-trained rowers. Analytic and classification methods that use the same plasma FT-IR spectra are described. Complete spectra (4000 to 500 cm(-1)) classifications led to a differentiation between most patients with type 1 diabetes and other subjects but not between control and trained subjects. Classification of defined absorption regions of spectra allowed different metabolic distinctions between populations. These were performed on the amide I and II absorption regions of proteins (1720 to 1480 cm(-1)); on the nu=CH, nu(as)CH(2), and nu(as)CH(3) absorption regions of lipids (3020 to 2880 cm(-1)); and on the nuC-O absorption region of saccharides (1300 to 900 cm(-1)). A classification that uses a combination of four absorption regions-nu=CH (3020 to 3000 cm(-1)), nu(as)CH(3) (3000 to 2950 cm(-1)), nuC-O (amide I: 1720 to 1600 cm(-1)), and nuC-O (carbonyle: 1300 to 900 cm(-1))-led to the formation of three exclusive clusters that comprised the defined populations. FT-IR spectroscopy is an exciting technique that allows a versatile approach to biologic samples from which analytic and statistical methods might be used for metabolic profile characterization and evaluation.

Adult↗

Butyrate impairs energy metabolism in isolated perfused liver of fed rats.

This study was designed to test the effects of short-chain fatty acids (SCFA) with an even number of carbon atoms on hepatic energy metabolism. The effect of the SCFA was evaluated by measuring liver ATP content and oxygen consumption. The ATP content was evaluated using (31)P nuclear magnetic resonance in isolated liver from fed rats. In addition, respiratory activity (VO(2)) was assessed using Clark electrodes. The livers were perfused with acetate, butyrate or a medium chain length fatty acid, octanoate, at a concentration of 0.05--5.0 mmol/L. The addition of each substrate enhanced the rate of the net ATP consumption (V(i)), establishing a new ATP steady state that required a perfusion time of > or = 20 min, dependent on the chain length and concentration of the fatty acid (FA). The initial V(i) was unchanged for acetate and the ATP level stabilized at 58% of the initial level. Both butyrate and octanoate induced a dose-dependent increase in V(i). This may reflect an ATP-consuming process for the intracellular pH regulation observed during the acidosis associated with the beta-oxidation pathway. At the new steady state, the ATP concentration was approximately 45% of the initial level for both FA. VO(2) was both rapidly and reversibly increased, and the change was a function of butyrate or octanoate concentration and of the chain length. K(m) values were similar for butyrate and octanoate. Because all of the effects were similar for butyrate and octanoate, in contrast to acetate, we suggest that the impairment of the energy metabolism by butyrate resulted from an increase in the FADH(2)/NADH ratio due to beta-oxidation. In conclusion, the difference in the hepatic oxidation pathways of two products of intestinal fermentation (acetate and butyrate) explains their different actions on energy metabolism.

Acetates↗

A randomized study comparing blood glucose control and risk of severe hypoglycemia achieved by non-programmable versus programmable external insulin pumps.

OBJECTIVE: To compare a non-programmable and a programmable insulin external pump using regular insulin on glycemic stability, the risk of severe hypoglycemia and metabolic control in type 1 diabetic patients. MATERIAL AND METHODS: Ten type 1 diabetic patients were involved in a randomized, crossover study comparing two periods of 3 months with continuous subcutaneous insulin infusion (CSII) either with a non-programmable insulin pump or a programmable insulin pump. Comparisons were made among mean blood glucose values before and after meals, at bedtime and at 2: 00 a.m.; the risk of severe hypoglycemia assessed by the low blood glucose index (LBGI); and HbA1c. RESULTS: Mean average blood glucose (BG) measurements were significantly lower with the programmable in comparison with the non-programmable insulin pump (respectively 157+/-78 vs. 165+/-79, p=0.034). While postprandial values for BG were not different between the two pumps, the use of the programmable pump resulted in a significant decrease in mean preprandial BG levels (140+/-68 vs. 150+/-73 mg/dl p=0.039). Conversely mean BG level was lower at 2 a.m. with the non-prgrammable pump (125+/-81 vs. 134 +/-93 mg/dl, p=0.02) but with a higher incidence of hypoglycemia. Mean LBGI was comparable with the two pumps (3.1+/-8.6 vs. 2.8+/-6.9, p=0.1). There was a 0.2% decrease in HbA1c during the programmable pump period that did not reach statistical significance (p=0.37). CONCLUSIONS: The present study suggests that programmable external insulin pumps, although more complex and more expensive than non-programmable insulin pumps, significantly reduce fasting glycemia during the day without increasing the risk of severe hypoglycemia and are safer during the night.

Adult↗

Liposomes as fatty acids carriers in isolated rat liver: effect on energy metabolism and on isolated mitochondria activity.

The effects of fatty acids (FA)-carrier, egg-lecithin liposomes (LIPO) as alternative to BSA, on ATP, glycogen and glucose contents in isolated perfused liver of fed rats were non-invasively studied using 31P/13C nuclear magnetic resonance (NMR). Oxidative phosphorylation was studied in isolated mitochondria from the same liver consecutively to the NMR experiments. ATP content decreased slowly and ATP turnover was similar during the perfusion with saline solution (KHB) or LIPO. However, LIPO induced an enhancement of respiratory control ratio in isolated mitochondria. Tissue glycogen and glucose content decreased when FA (linoleate or linolenate) were perfused with defatted BSA (3%) or LIPO (600 mg/l) whereas glucose excretion level was unchanged and lactate excretion tended to increase, reflecting changes in the cytosolic redox state and/or an enhancement of glycolysis. Addition of FA (0.5 or 1.5 mM) to LIPO caused a dramatic fall in liver ATP, a mitochondrial uncoupling and an impairment of the phosphorylation activity. Perfusion with FA (1.5 mM) carried by BSA significantly increased the ATP degradation without change of mitochondrial function. Owing to the higher affinity of BSA than LIPO for FA, these latter could be more easily released from complex LIPO-FA, increasing their uncoupling effect. Hence, the FA concentrations have to be largely decreased from the above currently used concentrations to avoid this effect. It will then be possible to minimize the effector action of FA and to study their more specific metabolic function as fuel. It was concluded that LIPO were appropriate carriers to study the different metabolic effects of FA.

Adenosine Triphosphate↗

Diabetes as a result of atypical anti-psychotic drugs--a report of three cases.

AIMS: Atypical anti-psychotic drugs (APDs) are widely used in psychotic disorders refractory to conventional neuroleptic agents. RESULTS: Three cases of new-onset diabetes are reported in Caucasian men who were on clozapine (one) or olanzapine (two) for 3-6 months. They had a distinct presentation: weight loss, ketosis (one ketoacidosis), severe hyperglycaemia requiring insulin therapy, and relative insulin deficiency as reflected by glucagon stimulatory tests. In all cases, insulin was stopped within 1 month after the APD was discontinued. CONCLUSIONS: Novel APDs not only induce diabetes as a result of weight gain in predisposed patients, but can also lead to a reversible state of insulin deficiency, and sometimes ketoacidosis.

Adult↗

Guillain-Barré syndrome occurring in two women after ketoacidosic comatose state disclosing an insulin-dependent diabetes mellitus.

We report two women who presented with a Guillain-Barré syndrome just after a ketoacidosic comatose state disclosing an insulin-dependent diabetes mellitus. One had characteristic clinical signs and the other had major motor involvement. At neurophysiologic investigations, one had typical demyelinating neuropathy whereas the second had mainly axonal degeneration. At ultrastructural examination of a peripheral nerve biopsy, features of macrophage-associated demyelination were present in both nerve specimens, thus confirming the diagnosis of acute inflammatory demyelinating polyneuropathy, i.e., Guillain-Barré syndrome. Prominent axonal involvement was also present in the motor nerves of the second patient. Insulin therapy had to be permanently continued and these two cases are quite different from the transient diabetes sometimes observed in certain cases of Guillain-Barré syndrome. Both the latter and insulin-dependent diabetes mellitus probably have auto-immune mechanisms. It is likely that in our two patients both auto-immune diseases were triggered by a common event. Such cases of Guillain-Barré syndrome have to be distinguished from other acute diabetic neuropathies.

Adult↗