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Biomedical subjects

A Tiengo

Publications and source records attributed to A Tiengo.

At least 91 records · Page 5Linked to original sources
PubMed1991

Effects of chronic alcohol intake on carbohydrate and lipid metabolism in subjects with type II (non-insulin-dependent) diabetes.

PURPOSE: To study the effects of chronic alcohol intake on carbohydrate and lipid metabolism in subjects with non-insulin-dependent (type II) diabetes (NIDDM). To also evaluate the effect of alcohol withdrawal on metabolic control. PATIENTS AND METHODS: The study group consisted of 46 alcohol-consuming patients with NIDDM (NIDDM-B group), 35 non-alcohol-consuming patients with NIDDM (NIDDM group), and 40 normal control subjects. All patients were admitted to the hospital. Carbohydrate and lipid metabolism was assessed in these individuals immediately on admission to the hospital and during the following days. RESULTS: In the NIDDM-B group, blood alcohol (ethyl alcohol) concentration was very low. However, chronic alcohol intake was associated with higher fasting and postprandial glucose concentrations and higher hemoglobin A1c. No significant differences were found in C-peptide levels. Moreover, higher concentrations of 3-hydroxybutyrate and free fatty acids were observed in the NIDDM-B group than in the NIDDM group. No differences were found in triglyceride concentrations, acid-base patterns, or electrolyte levels. The metabolic effects of alcohol completely waned after 3 days of complete withdrawal. CONCLUSION: Chronic alcohol intake causes deterioration in metabolic control of persons with NIDDM. The effects induced by alcohol are completely reversed after a few days of withdrawal. Strict metabolic assessment is necessary when alcohol is an important constituent of the diet.

3-Hydroxybutyric Acid↗
PubMed1991

No effects of high-fiber diets on metabolic control and insulin-sensitivity in type 1 diabetic subjects.

The metabolic effects of a three-month treatment with a high-fiber diet (15 grams of guar-gum added to a standard diet) were investigated in seven type 1 diabetic subjects, with a moderately poor metabolic control. HbA1c levels, daily insulin requirement, cholesterol, triglyceride, amino acid and intermediate metabolite concentrations were evaluated before and following the high fiber diet, both in the postabsorptive state at euglycemia and during a euglycemic, hyperinsulinemic, hyperaminoacidemic clamp. Insulin-mediated glucose utilization, an index of insulin-sensitivity, was also measured during the clamp. Following the diet, no differences in HbA1c levels (7.6 +/- 0.7%----7.3 +/- 0.6%), daily insulin requirement (50 +/- 5----51 +/- 3 U/d), triglyceride, amino acid and intermediary metabolite concentrations in the basal, euglycemic state, were observed. Only cholesterol concentrations decreased significantly (from 165 +/- 12 to 142 +/- 12 mg/dl, P less than 0.01) after the diet. During the clamp, the concentrations of all measured substrates were comparable before and after high fiber treatment. Insulin-mediated glucose disposal was also unchanged by guar-gum treatment. Patients' body weights were not modified by the diet. In conclusion, our study shows that a high fiber diet, obtained with the addition of 15 grams of guar-gum to a standard diet, is of no benefit to IDDM either as regards the metabolic control or insulin sensitivity. Only cholesterol levels were decreased. Therefore, the costs and benefits of these diets in the treatment of IDDM should be reconsidered.

Adult↗
PubMed1991

Glucose and lipid metabolism in non-insulin-dependent diabetes. Effect of metformin.

Basal and insulin-mediated glucose and free-fatty acid (FFA) metabolism was evaluated in 6 non-insulin-dependent diabetic patients (NIDDM) previously treated by diet, before and after 4 week metformin treatment (850 mg twice/day). On both occasions, an euglycemic stepwise insulin (20 and 40 mU/m2/min) clamp was performed along with primed-continuous infusion of 3-3H-glucose and 1-14C-palmitate and indirect calorimetry monitoring. FFA oxidation rate was measured from the rate of appearance of 14CO2. After metformin therapy, fasting plasma glucose, FFA, triglyceride, total cholesterol concentrations and HbA1c were all lowered (p less than 0.05-0.01) in the absence of any change in plasma insulin levels. Plasma FFA turnover rate (5.3 +/- 0.5 vs 3.9 +/- 0.8 mumol/kg/min; p less than 0.05) and FFA oxidation (0.93 +/- 0.12 vs 0.70 +/- 0.12 mumol/kg/min; p less than 0.05) were also lower after metformin treatment, while glucose oxidation increased from 0.9 +/- 0.2 vs 1.2 +/- 0.1 mg/kg/min. During the insulin clamp studies, whole body glucose disposal was higher both at the lower (2.1 +/- 0.4 vs 2.8 +/- 0.4 mg/kg/min) and higher insulin plateau (4.8 +/- 0.9 vs 6.3 +/- 0.9 mg/kg/min; p less than 0.01). Since no difference was apparent in glucose oxidation, the increase in glucose disposal was entirely accounted for by an improvement in non-oxidative glucose metabolism. Euglycemic hyperinsulinemia was followed by a reduction in plasma FFA concentration turnover rate that remained the same before and after metformin therapy. In conclusion, metformin treatment induces an improvement in glucose metabolism both in the basal and insulin-stimulated state.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1990

Partial recovery of insulin secretion and action after combined insulin-sulfonylurea treatment in type 2 (non-insulin-dependent) diabetic patients with secondary failure to oral agents.

Metabolic control, insulin secretion and insulin action were evaluated in seven Type 2 (non-insulin-dependent) diabetic patients with secondary failure to oral antidiabetic agents before and after two months of combined therapy with supper-time insulin (Ultratard: 0.4 U/kg body weight/day) plus premeal glibenclamide (15 mg/day). Metabolic control was assessed by 24 h plasma glucose, NEFA, and substrate (lactate, alanine, glycerol, ketone bodies) profile. Insulin secretion was evaluated by glucagon stimulation of C-peptide secretion, hyperglycaemic clamp (+ 7 mmol/l) and 24 h free-insulin and C-peptide profiles. The repeat studies, after two months of combined therapy, were performed at least 72 h after supper-time insulin withdrawal. Combining insulin and sulfonylurea agents resulted in a reduction in fasting plasma glucose (12.9 +/- 7 vs 10.4 +/- 1.2 mmol/l; p less than 0.05) and hepatic glucose production (13.9 +/- 1.1 vs 11.1 +/- 1.1 mumol.kg-1.min-1; p less than 0.05). Mean 24 h plasma glucose was also lower (13.7 +/- 1.2 vs 11.1 +/- 1.4 mmol/l; p less than 0.05). Decrements in fasting plasma glucose and mean 24 h profile were correlated (r = 0.90; p less than 0.01). HbA1c also improved (11.8 +/- 0.8 vs 8.9 +/- 0.5%; p less than 0.05). Twenty-four hour profile for NEFA, glycerol, and ketone bodies was lower after treatment, while no difference occurred in the blood lactate and alanine profile. Insulin secretion in response to glucagon (C-peptide = +0.53 +/- 0.07 vs +0.43 +/- 0.07 pmol/ml) and hyperglycaemia (freeinsulin = 13.1 +/- 2.0 vs 12.3 +/- 2.2 mU/l) did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1990

Insulin regulation of glucose and lipid metabolism in massive obesity.

Eight obese patients and 12 normal individuals underwent a euglycaemic insulin clamp (20 and 40 mU m2-1.min-1) along with continuous infusion of 3-3H-glucose and 1-14C-palmitate and indirect calorimetry. Basal plasma glucose concentration (4.7 +/- 0.3 vs 4.4 +/- 0.2 mmol/l) was similar in the two groups, whereas hepatic glucose production was slightly higher in obese individuals (1.11 +/- 0.06 vs 0.84 +/- 0.05 mmol/min) in spite of higher plasma insulin levels (17 +/- 2 vs 6 +/- 1 mU/l; p less than 0.01). Insulin inhibition of hepatic glucose production was impaired in obese subjects. Glucose disposal by lean body mass was markedly reduced both at baseline (11.7 +/- 1.1 vs 15.6 +/- 0.6 mumol.kg-1.min-1; p less than 0.05) and during clamp (15.0 +/- 1.1 vs 34.4 +/- 2.8 and 26.7 +/- 3.9 vs 62.2 +/- 2.8 mumol.kg-1.min-1; p less than 0.01) Oxidative (12.2 +/- 1.1 vs 17.8 +/- 1 and 16.1 +/- 1.1 vs 51.1 +/- 1.7 mumol.kg-1.min-1; p less than 0.05-0.002) and non-oxidative glucose metabolism (3.9 +/- 1.1 vs 15.0 +/- 2.8 and 12.8 +/- 3.3 vs 38.2 +/- 2.2 mumol.kg-1.min-1; p less than 0.01-0.001) were impaired. Basal plasma concentrations of non-esterified fatty acids (635 +/- 75 vs 510 +/- 71 mumol/l) and blood glycerol (129 +/- 17 vs 56 +/- 5 mumol/l; p less than 0.01) were increased in obese patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Effects of insulin on whole body and forearm leucine and KIC metabolism in type 1 diabetes.

To investigate whole body rates of appearance (Ra) and forearm metabolism of leucine and alpha-ketoisocaproate (KIC) in type 1 diabetes, before and after insulin administration, seven diabetic subjects were studied in the postabsorptive state with primed-constant infusions of L-[4,5-3H]leucine and [1-14C]KIC, and forearm arterial deep-venous catheterization. This combined technique allowed the selective quantitation of the two processes regulating forearm leucine and KIC metabolism (release and uptake) that may occur simultaneously. Before insulin (arterial plasma glucose, 284 +/- 24 mg/dl; leucine, 215 +/- 24 mumol/l; KIC, 42 +/- 3 mumol/l) forearm leucine and KIC release exceeded uptake slightly but significantly (P less than 0.05). During a 180-min insulin infusion, arterial glucose (144 +/- 27 mg/dl) and leucine concentrations (130 +/- 15 mumol/l) decreased (P less than 0.05 or less vs. base line) toward normal, whereas KIC did not change (33 +/- 4 mumol/l, NS). However, no net uptake of either leucine or KIC across the forearm was detected at any time point. In contrast, a significant net release of these substrates occurred throughout the insulin infusion. By the end of the hormone administration, whole body leucine and KIC Ra decreased 17 and 33%, respectively (P less than 0.01). However, forearm uptake and release of leucine and KIC did not significantly change with respect to base line. The fraction of whole body leucine released from estimated total muscle mass did not change (54 to 48%, NS) before vs. after insulin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Glucose turnover and recycling in diabetes secondary to total pancreatectomy: effect of glucagon infusion.

This study was designed to evaluate whether chronic deficiency of pancreatic glucagon in patients with diabetes secondary to total pancreatectomy (PX) is responsible for the commonly observed increase in blood concentrations of gluconeogenic precursors (alanine, lactate, and pyruvate). Seven PX patients were studied on two different occasions: 1) after an overnight insulin infusion (0.15 mU/kg.min) and 2) after an overnight insulin/glucagon infusion (2 ng/kg.min). Five type 1 diabetic individuals were also studied after a similar overnight insulin infusion. In the morning of each study day, [6-3H]glucose and [1-14C]glucose were rapidly injected for determination of total glucose turnover rate [( 6-3H]glucose) and glucose recycling (difference between [6-3H]glucose and [1-14C]glucose turnover rate). Basal concentrations of hormones, glucose, and intermediary metabolites were measured. After overnight insulin infusion, plasma glucose concentration (3.8 +/- 0.4 vs. 6.8 +/- 1.4 mmol/L), turnover rate (8.4 +/- 1.0 vs. 13.7 +/- 1.9 mumol/kg.min), and percent glucose recycling (5.6 +/- 3.9% vs. 19.0 +/- 3.8%) were significantly lower in PX patients than in type 1 diabetic individuals (P less than 0.05-0.01). On the contrary, blood alanine (459 +/- 93 vs. 263 +/- 28 mumol/L), lactate (1157 +/- 109 vs. 818 +/- 116 mumol/L), and pyruvate (71 +/- 8 vs. 42 +/- 3 mumol/L) were significantly higher than those values in type 1 diabetic patients (P less than 0.05-0.01). Insulin/glucagon infusion increased plasma glucose concentration (8.7 +/- 1.5 mmol/L), total turnover (18.1 +/- 1.7 mumol/kg.min), and percent recycling (20.4 +/- 6.6%) to values similar to those in type 1 diabetic subjects. The change in glucose metabolism was associated with a significant drop in blood concentrations of alanine (179 +/- 24 mumol/L), lactate (611 +/- 25 mumol/L), and pyruvate (30 +/- 3 mumol/L; all P less than 0.05-0.01 vs. insulin infusion alone). In PX patients, the glucose turnover rate was inversely correlated with blood concentrations of both alanine (r = 0.67) and lactate (r = 0.71; P less than 0.01). In conclusion, chronic deficiency of pancreatic glucagon in PX patients 1) is associated with a decreased rate of glucose turnover, 2) causes a marked impairment in glucose recycling (an index of the activity of hepatic gluconeogenesis), and 3) increases blood concentrations of alanine, lactate, and pyruvate. All abnormalities are reversed by glucagon.

Adult↗
PubMed1989

The medium-term effect of natural or extractive dietary fibres on plasma amino acids and lipids in type 1 diabetics.

We evaluated the effect of a diet rich in natural (NF) or extractive fibres (guar gum) on 12 male IDD (insulin-dependent diabetes) out-patients. The treatment lasted for 2 months. During the first month the patients were on an isocaloric diet containing 30 g of fibres and then they were randomly subdivided into two groups. One group followed an isocaloric diet rich in fibres (70 g/day), the second group an isocaloric diet enriched by guar (9 g of guar added to 30 g of natural fibres/day). Reduced serum levels of HbA1c and several amino acids showed that metabolic control significantly improved under each dietary regimen.

Adult↗
PubMed1989

Leucine kinetics and the effects of hyperinsulinemia in patients with Cushing's syndrome.

As muscle wasting and resistance to insulin-mediated glucose utilization are features of Cushing's syndrome (CS), we examined glucose and amino acid metabolism in six patients with CS and six normal subjects before and during euglycemic hyperinsulinemic clamp studies (plasma insulin concentrations, approximately 0.36, approximately 0.65, and approximately 10.05 mmol/L). The two groups had similar body mass index values. In the postabsorptive state, leucine and alpha-ketoisocaproate (KIC) rates of appearance (Ra), KIC oxidation, and nonoxidized leucine-carbon flux, an index of leucine entering protein (Leu----P), were comparable in CS patients [2.38 +/- 0.14 (+/- SE), 0.22 +/- 0.04, and 2.16 +/- 0.12 mumol/kg.min) and in normal subjects (2.73 +/- 0.25, 0.17 +/- 0.02, and 2.59 +/- 0.22 mumol/kg.min). During the euglycemic clamp studies the leucine and KIC Ra values, KIC oxidation, and Leu----P decreased to a similar extent in both groups. In contrast, insulin-mediated glucose utilization was impaired in the CS patients at each clamp step (P less than 0.05). In summary, postabsorptive whole body leucine metabolism is normal in patients with CS and is normally suppressed by hyperinsulinemia, indicating a dissociation in insulin sensitivity with respect to glucose and amino acid metabolism.

Adolescent↗
PubMed1989

Effects of different insulin administrations on plasma amino acid profile in insulin-dependent diabetic patients.

It has long been recognized that diabetes mellitus is characterized by alterations in amino acid metabolism. Our aim was to evaluate the fasting amino acid concentrations in insulin-dependent diabetic subjects treated with different kinds of insulin therapy and with respect to the resulting different metabolic control. Four groups of patients were studied: Group 1: eight type 1 diabetic patients with two daily insulin injections; Group 2: eight type 1 diabetic patients with continuous subcutaneous insulin infusion; Group 3: five type 1 diabetic patients with continuous intraperitoneal insulin infusion; Group 4: six patients with total pancreatectomy. In all patients fasting amino acid profile was determined. Group 1 was also studied after 24 hr insulin withdrawal and after acute normalization of glycaemia. Our data demonstrated that the patients with a mild hyperglycaemia showed a significant increase in plasma amino acid levels. The continuous subcutaneous or intraperitoneal insulin infusion normalized amino acid profile at the expense of peripheral hyperinsulinemia, suggesting the presence of insulin resistance with regard of amino acid metabolism. The acute normoglycaemia demonstrated that plasma branched chain amino acid levels are more sensitive than plasma glucose to insulin action. Moreover, the amino acid pattern of euglycaemic total pancreatectomized patients suggested that a basal level of glucagon is essential in regulating glycogenic amino acid plasma concentrations.

Amino Acids↗
PubMed1988

Metabolic control during total parenteral nutrition: use of an artificial endocrine pancreas.

The metabolic impact of total parenteral nutrition (TPN) was evaluated in nine subjects who underwent esophagogastroplasty for esophageal carcinoma. On the second day after operation all subjects were connected to an artificial endocrine pancreas. In four patients only glucose was infused (5.5 mg/kg X min). The remaining five subjects received glucose (4.0 mg/kg X min), amino acid (0.5 mg/kg X min), and lipid emulsion (0.6 mg/kg X min). Plasma glucose concentration was kept constant over 24 hours. However, both insulin requirement (111 +/- 15 v 70 +/- 2 mU/kg X h) and plasma insulin level (99 +/- 15 v 30 +/- 7 microU/mL; P less than .01) were higher during combined TPN. Blood lactate concentration was higher during glucose infusion (P less than .05). No difference was found in blood concentrations of pyruvate, alanine, and ketone bodies. Both glycerol and FFA were higher during combined TPN. The ratio between glucose infusion rate and the average plasma insulin level was calculated as an index of insulin-mediated glucose metabolism; G/I X 100 was markedly reduced during combined TPN (4.5 +/- 0.8 v 20.7 +/- 3.7; P less than .05). Plasma FFA levels were positively correlated with plasma insulin concentration (r = .76) and inversely correlated to G/I X 100 (r = -.73; both P less than .05). In conclusion, during combined TPN a state of insulin resistance is induced and more insulin is required to achieve a normal glucose utilization.

Blood Glucose↗
PubMed1987

Insulin receptors on circulating blood cells from patients with pancreatogenic diabetes: a comparison with type I diabetes and normal subjects.

We studied 125I-insulin binding to erythrocytes from 14 patients with diabetes secondary to chronic pancreatitis or pancreatectomy and compared the results with those found in 10 patients with type I diabetes and 25 normal controls. Patients with pancreatogenic diabetes had higher 125I-insulin binding and enhanced tissue sensitivity to exogenous insulin measured with the glucose clamp technique as compared with patients with type I diabetes. Similar binding data were obtained with monocytes from 3 patients with pancreatogenic diabetes. The increase in insulin binding seemed due mainly to an increase in receptor number. The increase in insulin binding to cells from patients with pancreatogenic diabetes in comparison with cells from normal subjects was also seen in young-erythrocyte-rich fractions and in old-erythrocyte-rich fractions obtained from the mixed population of circulating erythrocytes by centrifugation in density gradient of Percoll-Pielografin. These data, in the absence of any sign of major hematological disorders, suggest that the increase in insulin receptors seen in erythrocytes and in monocytes from patients with pancreatogenic diabetes, can mirror a general phenomenon on tissues throughout the body, including major target cells for insulin and correlate with the heightened sensitivity to insulin characteristic of these patients. In conclusion, patients with pancreatogenic diabetes have increased insulin binding as compared to controls and to patients with type I diabetes with chronic hypoinsulinemia of the same degree. Thus, in addition to insulin deficiency, other factor (s), such as glucagon deficiency, are responsible for the clinical and metabolic differences between these two conditions of insulin deficiency.

Blood Cells↗
PubMed1987

Differential effects of hyperinsulinemia and hyperaminoacidemia on leucine-carbon metabolism in vivo. Evidence for distinct mechanisms in regulation of net amino acid deposition.

The effects of physiologic hyperinsulinemia and hyperaminoacidemia, alone or in combination, on leucine kinetics in vivo were studied in postabsorptive healthy subjects with primed-constant infusions of L-[4,5-3H]leucine and [1-14C]alpha-ketoisocaproate (KIC) under euglycemic conditions. Hyperinsulinemia (approximately 100 microU/ml) decreased (P less than 0.05 vs. baseline) steady state Leucine + KIC rates of appearance (Ra) from proteolysis, KIC (approximately leucine-carbon) oxidation, and nonoxidized leucine-carbon flux (leucine----protein). Hyperaminoacidemia (plasma leucine, 210 mumol/liter), with either basal hormone replacement or combined to hyperinsulinemia, resulted in comparable increases in leucine + KIC Ra, KIC oxidation, and leucine----protein (P less than 0.05 vs. baseline). However, endogenous leucine + KIC Ra was suppressed only with the combined infusion. Therefore, on the basis of leucine kinetic data, hyperinsulinemia and hyperaminoacidemia stimulated net protein anabolism in vivo by different mechanisms. Hyperinsulinemia decreased proteolysis but did not stimulate leucine----protein. Hyperaminoacidemia per se stimulated leucine----protein but did not suppress endogenous proteolysis. When combined, they had a cumulative effect on net leucine deposition into body protein.

Amino Acids↗
PubMed1987

Alcohol impairs insulin sensitivity in normal subjects.

The effects of alcohol on insulin action are not yet clearly established. To assess the effects of intravenously administered ethanol on insulin mediated glucose disposal, euglycaemic clamps at 3 different plasma insulin levels and insulin receptor binding studies on circulating monocytes after alcohol infusion were performed. Ethanol infusion leads to a significant reduction of insulin mediated glucose disposal (7.08 +/- 0.4 vs 8.6 +/- 0.6 mg/Kg/min; 9.8 +/- 0.7 vs 13.4 +/- 0.7; 14.7 +/- 0.7 vs 18.1 +/- 0.7 at 33, 73 and 760 mU/m2/min insulin infusion rate respectively). Monocyte insulin-receptor binding was decreased in all the subjects from 30 to 60% after ethanol infusion. These results demonstrate that alcohol can adversely influence the insulin mediated glucose disposal.

Blood Glucose↗