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Biomedical subjects

A Tiengo

Publications and source records attributed to A Tiengo.

At least 55 records · Page 3Linked to original sources
PubMed1996

Gliclazide potentiates suppression of hepatic glucose production in non-insulin-dependent diabetic patients.

The mechanism of the hypoglycemic action of gliclazide was evaluated in 17 diet-treated non-insulin-dependent diabetes mellitus (NIDDM) patients. In study A, five patients received a 240-minute glucose infusion along with [3-3H]glucose infusion. In study B, seven patients received a 240-minute isoglycemic insulin clamp along with [3-3H]glucose infusion. And in study C, five patients received a somatostatin infusion with basal replacing doses of insulin and glucagon. The three studies (A, B, and C) were repeated twice. Gliclazide (240 mg orally) was administered on one occasion, and placebo was given on the second occasion. Basal hepatic glucose production (HGP) and utilization and plasma glucose, insulin, C-peptide, glucagon, and free fatty acid (FFA) concentrations were similar before administration of gliclazide and placebo. In study A, plasma glucose, its incremental area, and HGP were reduced by gliclazide administration (all P < .05), but glucose utilization was not significantly affected. The increase in plasma insulin and C-peptide concentrations was similar with gliclazide and placebo, although the plasma insulin to glucose ratio was increased with gliclazide. HGP decremental area was correlated with the reduction in plasma glucose incremental area (r = -.63, P < .05). In study B, gliclazide administration produced a larger suppression of HGP, but the overall rate of glucose utilization was not different in the two studies. In study C, plasma glucose concentration and HGP progressively decreased in both studies, without a difference between gliclazide and placebo. These results suggest that under conditions of hyperglycemia and hyperinsulinemia gliclazide elicits a larger suppression of HGP.

Blood Glucose↗
PubMed1996

The role of substrates in the regulation of protein metabolism.

Substrates are powerful modulators of amino acid and protein turnover in vivo (Table 4). Intravenous infusions of amino acids exert a protein-anabolic effect, because they directly inhibit endogenous protein degradation and stimulate protein synthesis at the whole-body level. A stimulation of protein synthesis has been observed also at the forearm level. These changes resulted in an improvement of body and tissue protein balance, which is the ultimate goal of any nutritional intervention aimed at preserving body protein stores. In humans acute intravenous infusions of carbohydrates do not appear to affect either protein degradation or leucine oxidation. However, animal studies support the view that glucose availability spares essential amino acids at least in the fetus. The effects of hypercaloric refeeding with high-carbohydrate diets may, however, result in increased protein turnover. Lipids, in the form of long-chain fatty acids, inhibit endogenous protein breakdown and may suppress leucine oxidation in the whole body. They do not affect protein synthesis. In contrast, medium-chain fatty acids apparently increased leucine oxidation, and therefore increased net protein catabolism. Ketone bodies may be anabolic provided that fatty acid concentrations are not concurrently decreased.

Amino Acids↗
PubMed1996

Response of phenylalanine and leucine kinetics to branched chain-enriched amino acids and insulin in patients with cirrhosis.

BACKGROUND & AIMS: We tested the effects of branched chain-enriched, aromatic-deficient amino acids with insulin to correct the altered protein turnover as well as phenylalanine (Phe) and leucine (Leu) rate of appearance in compensated cirrhotics and controls. METHODS: Phe and Leu tracers were infused both before and following intravenous amino acid administration with insulin and euglycemic clamp. RESULTS: In cirrhosis, fasting whole-body protein synthesis and protein degradation were normal; Phe rate of appearance was greater (P<0.05), whereas Leu rate of appearance/Phe rate of appearance ratio was approximately 35% less than in controls (P<0.001). Following the infusion, protein synthesis did not increase (+1% +/ 5% [NS] vs. +21% +/- 5% [P<0.05] in controls); protein degradation was more suppressed, whereas protein balance increased normally. Total Phe rate of appearance (0.91 +/- 0.13 micromol x kg-1 x min-1) and Leu/Phe disposal ratio (3.53 +/- 0.36) were nearly normalized (fasting controls, 0.68 +/- 0.07 micromol x kg-1 x min-1 and 2.87 +/- 0.14 micromol x kg-1 x min-1, respectively; P>0.05). However, Leu/Phe endogenous rate of appearance ration remained approximately 50% less (1.56 +/- 0.31 vs. 2.87 +/- 0.14; P<0.004) than in controls. CONCLUSIONS: Following this combined infusion in cirrhosis, net protein deposition increased normally despite a blunted response of protein synthesis. Phe and Leu to Phe peripheral disposal were near normalized; however, the exaggerated endogenous Phe production was not corrected entirely.

Amino Acids, Branched-Chain↗
PubMed1996

Ethanol impairs insulin-mediated glucose uptake by an indirect mechanism.

The effect of ethanol (ETOH) on muscle metabolism was assessed in both normal (NC) and noninsulin-dependent (NIDDM) subjects in the basal state and during isoglycemic hyperinsulinemia (450 pmol/L) clamp studies carried out either with systemic (NC, n = 5; NIDDM, n = 5) or intrabrachially (NC, n = 5; NIDDM, n = 5)ETOH infusion. On a repeat study, each subject underwent the same experimental procedures, except that saline was infused instead of ETOH. Systemic ETOH significantly decreased whole body glucose disposal in both NC and NIDDM patients. In NC, ETOH infusion decreased basal forearm glucose uptake (FGU) from 1.22 +/- 0.20 to 0.32 +/- 0.04 mumol/min.100 mL tissue (P < 0.01), whereas in NIDDM, this decrement was not significant (from 0.95 +/- 0.31 to 0.66 +/- 0.23). With saline infusion, hyperinsulinemia significantly stimulated FGU to 4.09 +/- 0.46 mumol/min.100 mL tissue in NC and to 2.50 +/- 0.76 in NIDDM. During ETOH, FGU was depressed by 81% in NC (delta = 3.32 mumol/min.100 mL tissue) and by 48% (P < 0.05) in NIDDM (delta = 1.21 mumol/min.100 mL tissue). Local ETOH infusion did not affect FGU in either NC (1.18 +/- 0.23 vs. 1.1 +/= 0.11 mumol/min.100 mL tissue in the baseline condition and 4.12 +/- 0.65 vs. 3.97 +/- 0.35 in insulin-stimulated conditions) or NIDDM (1.05 +/- 0.29 vs. 1.1 +/- 0.19 mumol/min.100 mL tissue in baseline condition and 2.72 +/- 0.82 vs. 2.83 +/- 0.51 in insulin-stimulated conditions) subjects. With systemic ETOH, but not local infusion, there was a reduction in baseline plasma free fatty acid level and an increase in blood lactate concentration during isoglycemic hyperinsulinemia. In summary, systemic ETOH infusion impairs both whole body and forearm glucose uptake in NC and NIDDM subjects; this effect was more apparent in NC than in NIDDM at both the whole body and forearm level. On the contrary, intrabrachial ETOH infusion did not affect forearm glucose balance in either group. These results suggest that the reduction in muscle glucose disposal associated with increased systemic ETOH concentrations is not caused by a direct ETOH effect on muscle glucose metabolism.

Adult↗
PubMed1996

Hyperglucagonemia stimulates phenylalanine oxidation in humans.

Glucagon stimulates in vitro liver phenylalanine (Phe) degradation, thus inducing net protein catabolism. Whether these effects occur also in vivo in humans is not known. Therefore, we studied the effects of physiological hyperglucagonemia on Phe rate of appearance (Ra), hydroxylation, and oxidation in seven normal volunteers during infusions of somatostatin with replacement doses of insulin and growth hormone. Steady-state Phe kinetics were evaluated using the L-[1-14C]Phe tracer both at the end of a 3-h basal glucagon replacement period (glucagon concentration: 212 +/- 115 ng/l) and after a 3-h hormone infusion at the rate of approximately 3 ng x kg-1 x min-1 (--> 654 +/- 280 ng/l). Hyperglucagonemia did not change plasma Phe concentration and Ra but increased Phe oxidation by approximately 30% (P < 0.01). Oxidation was also increased by approximately 24% (P < 0.01) using plasma [14C]tyrosine (Tyr) specific activity as a precursor pool. Phe hydroxylation to Tyr estimated by assuming a fixed ratio of Tyr to Phe Ra (0.73) did not change. Nonhydroxylated Phe disposal decreased by approximately 6% (P = 0.08). These data show that in humans in the postabsorptive state, hyperglucagonemia, with near maintenance of basal insulin and growth hormone concentrations, stimulates Phe oxidation but not Phe hydroxylation, suggesting a different regulation of these two Phe catabolic steps. Glucagon may also reduce Phe availability for protein synthesis.

Adult↗
PubMed1996

The hemodynamic abnormalities in short-term insulin deficiency: the role of prostaglandin inhibition.

It has been suggested that the hemodynamic derangements present in diabetic ketoacidosis are the results not only of profound volume depletion but also of the effects of increased production of vasodilating prostaglandins (PGs), principally PGI2, released by adipose tissue. In animal and in vitro models, prostaglandin synthesis is increased during insulin deficiency. We assessed the effects of short-term ketosis on the metabolic and hemodynamic variables of 10 IDDM patients free from long-term complications and of 9 normal control subjects after a 7-day randomized double-blind indomethacin (INDO) (50 mg q.i.d.) or placebo treatment period. Calf blood flow (CBF), postocclusive reactive hyperemia (PORH), and recovery half-time (an index of overall perfusion) after PORH were measured by plethysmography. Left ventricular and myocardial functions were also studied in each different condition during placebo and INDO treatment in IDDM patients. During placebo treatment, the increase in CBF during ketosis was higher (1.75 +/- 0.29 ml / min / 100 ml muscle) than during INDO (0.85 +/- 0.17 ml / min) / 100 ml muscle; P = 0.007). PORH was similar in baseline conditions, during ketosis, and in recovery in both the placebo and INDO arms. Recovery half-time significantly increased during placebo (10 +/- 2; 200%; P < 0.01) but not during INDO (1 +/- 1; 106%; NS) treatment. In normal control subjects, insulin deficiency did not induce any significant effect on hemodynamic variables. In IDDM patients, during placebo treatment, ketosis increased both the cardiac index (from 3.4 +/- 0.7 to 4.1 +/- 0.81 / min / m; P < 0.01) and the stroke index (from 42 +/- 8 to 49 +/- 7 ml/m2; P < 0.01) without changes in left ventricular ejection fraction but with a significant increase in both left and right ventricular end-diastolic volumes. Metabolic recovery induced a normalization of these parameters. INDO treatment significantly blunted these alterations. In summary, we showed that during acute insulin deficiency, INDO-sensitive mechanisms mediate vascular disturbances. Moreover, INDO treatment was capable of completely preventing the cardiac venous return and the left ventricular alterations. INDO does not interfere with the overall ketogenetic process or with insulin-induced metabolic recovery.

3-Hydroxybutyric Acid↗
PubMed1996

[Lipid peroxidation and LDL modifications in nondiabetic patients with ischemic heart disease: the role of insulin action].

BACKGROUND: Nondiabetic patients with advanced coronary artery disease (CAD) were assessed for lipid peroxidation, LDL modifications and insulin action. Twenty-four patients and 10 normal controls were studied. METHODS: Insulin tolerance test (Kitt), glucose, insulin lipoproteins, electronegatively charged, modified, low density lipoproteins (LDL-) and the thiobarbituric acid reactivity (TBARS), as an index of lipid peroxidation, were determined. RESULTS: No difference was observed in insulin action (determined by insulin tolerance test) between patients with CAD (3.31 +/- 0.28%/min; range 0.73-6.13) and normal controls (3.59 +/- 0.42; range 1.76-6.06). The percentage of modified, electronegative LDL (LDL -) was higher in patients with CAD (0.5 +/- 0.48%; range 1.3-9.2) than that of controls (2.80 +/- 0.33; range 1.00-4.00; p = 0.013). TBARS were significantly (P = 0.043) higher in CAD patients (3.49 +/- 0.17 nmol/ml; range 2.4-5.5) than normal controls (1.47 +/- 0.12; range 1.07-2.10). A significantly negative correlation was observed between Kitt and TBARS (r= - 0.48; p = 0.016), and a significant (r = 0.46; p = 0.022) positive correlation was observed between plasma glucose and TBARS. On the contrary no correlation has been observed between LDL- and TBARS. CONCLUSIONS: We conclude that in patients with advanced coronary artery disease: A) there are increased circulating levels of modified low density lipoprotein; B) there is evidence of increased lipid peroxidation. This latter process is significantly influenced by the degree of insulin action.

Blood Glucose↗
PubMed1995

Insulin action and glucose metabolism are improved by gemfibrozil treatment in hypertriglyceridemic patients.

The aim of this study was to determine whether gemfibrozil-mediated decrease in very low density lipoprotein triglyceride (VLDL-TG) concentration is accompanied by an improvement in overall glucose metabolism in hypertriglyceridemic patients. We assessed this hypothesis in 7 hypertriglyceridemic without (HTG) and in 11 hypertriglyceridemic with noninsulin-dependent diabetes mellitus (NIDDM-HTG) who followed three-months treatment either with the drug or with placebo. Placebo VLDL-TG concentrations in both HTG (3.82 +/- 0.92 mmol/l (mean +/- S.D.) vs. 3.91 +/- 1.01 mmol/l) and in NIDDM-HTG (6.62 +/- 3.93 mmol/l vs. 6.84 +/- 4.16 mmol/l) were not different from baseline values, whereas gemfibrozil decreased VLDL-TG in both groups (1.84 +/- 0.56 mmol/l, P < 0.001 for HTG, and 1.93 +/- 2.68 mmol/l, P = 0.013 in NIDDM-HTG). In both groups, gemfibrozil treatment was associated with an improvement in fasting plasma glucose levels (from 5.85 +/- 0.92 mmol/l to 4.87 +/- 0.40 mmol/l in HTG, P = 0.001, and from 11.47 +/- 2.92 mmol/l to 9.56 +/- 3.41 mmol/l in NIDDM-HTG, P = 0.042). In NIDDM-HTG, gemfibrozil treatment was associated with a significantly lower 2 h-postprandial plasma glucose level (9.87 +/- 3.63 vs. 13.09 +/- 3.62, P = 0.05). A significant decrease in fasting free fatty acids (FFA) level was observed during gemfibrozil treatment in both groups, whereas in NIDDM-HTG, a significant drop of these substrates was observed in both fasting and postprandial conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1995

Effect of low-dose ramipril on microalbuminuria in normotensive or mild hypertensive non-insulin-dependent diabetic patients. North-East Italy Microalbuminuria Study Group.

Microalbuminuria predicts early mortality and renal disease in non-insulin-dependent diabetic patients. In insulin-dependent diabetic patients, angiotensin converting enzyme inhibition decreases microalbuminuria and retards the progression of renal disease. The aim of this study was to evaluate the effect of low dose ramipril on albumin excretion rate (AER) and blood pressure in non-insulin-dependent diabetic patients with persistent microalbuminuria (AER > 20 < 200 micrograms/min) and normal blood pressure or mild hypertension. The study was a randomized, double-blind, placebo-controlled clinical trial of 6 months duration at 14 hospital-based diabetes centers in northeastern Italy. Blood pressure, plasma glucose, and body weight were determined every month; AER, serum creatinine, glycosylated hemoglobin, and plasma lipids at baseline, after 1 month, and at the end of the study. Of 122 non-insulin-dependent diabetic patients randomly allocated in blocks of four to receive either ramipril (1.25 mg/day) or placebo, 108 (54 in the ramipril group and 54 in the placebo group) completed the study. At baseline, age, duration of diabetes, body mass index, and glycosylated hemoglobin were similar in the two groups and remained unchanged throughout the study. In the placebo group, AER rose from a baseline median of 65 micrograms/min (range 53 to 76, 95% confidence Interval) to 72 micrograms/min (57 to 87) and to 83 micrograms/min (62 to 104) after 1 and 6 months, respectively, but fell from 62 micrograms/min (48 to 76) to 45 micrograms/min (33 to 57) and to 53 micrograms/min (38 to 69), respectively, in the ramipril group, a significant difference between the groups (P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Surgical removal of insulinoma restores glucose recovery from hypoglycaemia but does not normalize insulin action.

In the present study we have evaluated the effects of chronic hyperinsulinaemia secondary to insulinoma, on insulin sensitivity and on counter-regulatory responses to hypoglycaemia. We studied six patients (M/F = 3/3; age = 40 +/- years), before and 6-9 months after surgical ablation of the neoplasia, by means of an euglycaemic-hyperinsulinaemic clamp (1 mU kg-1 min-1). Seven normal subjects (M/F = 4/3; age = 38 +/- 6 years) underwent the same experimental study as the control subjects. In insulinoma patients after 100 min of the euglycaemic-hyperinsulinaemic clamp, glycaemia was allowed to drop to a minimum value of 1.9 mmol L-1, and recovery evaluated after interrupting insulin infusion. During the entire study, 3-3H-glucose was infused to determine hepatic glucose production and glucose utilization. Surgical removal of the pancreatic adenoma was followed by a reduction in body weight (BMI = 25.7 +/- 1.9 vs. 23.0 +/- 1.6 kg m-2; P < 0.05), normalization of fasting plasma levels of glucose (2.94 +/- 0.16 vs. 4.83 +/- 0.11 mmol L-1), insulin (162 +/- 24 vs. 48 +/- 12 pmol L-1) and of basal hepatic glucose production (7.6 +/- 0.7 vs. 12.2 +/- 1.11 mumol kg-1 min-1). Before the operation, insulin-mediated glucose disposal was significantly lower than in the controls (30.8 +/- 3.1 vs. 49.1 +/- 3.1 mumol kg-1 min-1). Six to nine months after surgical removal of the adenoma, glucose utilization was unchanged (30.5 +/- 3.3 mumol kg-1 min-1) and still significantly lower than in controls (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Basal plasma insulin levels exert a qualitative but not quantitative effect on glucose-mediated glucose uptake.

UNLABELLED: We assessed the effect of hyperglycemia on glucose uptake in the presence of normal basal insulin levels or somatostatin-induced hypoinsulinemia in seven normal volunteers during a 200-min hyperglycemic clamp (+ 9 mmol/l) carried out with [3-3H]glucose and indirect calorimetry. Hyperglycemia increased glucose uptake to 22.4 +/- 2.6 and 21.3 +/- 1.6 mumol.kg-1.min-1 with and without insulin replacement, respectively. Normoinsulinemia increased glucose oxidation (delta = + 4.5 +/- 0.6 mumol.kg-1.min-1) and nonoxidative glucose metabolism (delta = + 5.2 +/- 1.7 mumol.kg-1.min-1), whereas with insulinopenia, glucose oxidation did not change (delta = -0.3 +/- 0.6 mumol.kg-1.min-1), and nonoxidative glucose metabolism increased (delta = + 48.7 +/- 0.8 mumol.kg-1.min-1). Nonoxidative glucose metabolism was higher during insulinopenic (13.5 +/- 1.8 mumol.kg-1.min-1) than normoinsulinemic hyperglycemia (9.8 +/- 2.7 mumol.kg-1.min-1; P < 0.01). Plasma FFA concentration and lipid oxidation were higher with insulinopenia. Blood lactate and alanine concentrations were greater with normoinsulinemia. IN CONCLUSION: 1) hyperglycemia promotes glucose uptake by stimulating both nonoxidative and oxidative glucose disposal; 2) the ability of hyperglycemia to enhance total body glucose uptake is similar with and without normoinsulinemia; 3) although acute insulinopenia does not impair the ability of hyperglycemia to stimulate glucose uptake, it plays a critical role in determining the intracellular metabolic fate of glucose taken up in response to hyperglycemia.

Adult↗
PubMed1995

Regulation of postprandial whole-body proteolysis in insulin-deprived IDDM.

Suppression of tissue proteolysis is an important mechanism of postprandial protein anabolism, and it may be mediated by insulin, hyperaminoacidemia, or both. To evaluate whether insulin is essential in the regulation of this process, we have investigated the effect of mixed-meal ingestion on whole-body protein breakdown in insulin-deprived insulin-dependent diabetes mellitus (IDDM) patients and normal control subjects. Endogenous phenylalanine and leucine rate of appearance (Ra) from proteolysis were measured at steady-state conditions using a multiple stable isotope technique before and after the constant administration of a synthetic mixed meal. In the postabsorptive state, the IDDM patients exhibited accelerated intracellular leucine Ra (IDDM, 2.64 +/- 0.19 mumol.min-1.kg-1; control, 2.02 +/- 0.08 mumol.min-1.kg-1; P < 0.05) and plasma phenylalanine Ra (IDDM, 0.73 +/- 0.03 mumol.min-1.kg-1; control, 0.61 +/- 0.04 mumol.min-1.kg-1; P < 0.05). During meal ingestion, endogenous phenylalanine and leucine Ra values were suppressed in both the insulin-deficient IDDM (P < 0.05) and control subjects (P < 0.05). Although postmeal endogenous leucine and phenylalanine Ra values remained greater (P < 0.05) in IDDM, the delta changes from the basal endogenous leucine Ra (IDDM, -0.56 +/- 0.11 mumol.min-1.kg-1; control, -0.56 +/- 0.09 mumol.min-1.kg-1) and phenylalanine Ra (IDDM, -0.13 +/- 0.01 mumol.min-1.kg-1; control, -0.14 +/- 0.02 mumol.min-1.kg-1) were similar in both groups. In the IDDM patients, the postmeal increases from the basal leucine concentration were onefold greater (P < 0.05) than in the control-subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Sequelae of acute hypoglycaemia on 24 hour blood pressure and metabolic parameters in normal and type 1 (insulin-dependent) diabetic individuals.

This study was performed to assess possible delayed after-effects of acute hypoglycaemia on blood pressure (BP) and heart rate (HR) over a 24-h period. Eleven insulin-dependent diabetic patients and 11 sex, age, and body mass index matched non-diabetic subjects were studied. Blood pressure was measured using a non-invasive ambulatory blood pressure monitor following acutely induced hypoglycaemia in the morning. No significant differences were observed in 24-h systolic and diastolic BP and HR in either groups, between the day when hypoglycaemia was induced and the day when plasma glucose was kept normal. In diabetic patients, hypoglycaemia induced a temporary but significant fall in mean BP (-7 +/- 1 mmHg vs -2 +/- 2; p < 0.05). Plasma glucose levels were significantly higher in insulin-dependent diabetic patients following hypoglycaemia than in those observed during the reference test. This study demonstrates that acute hypoglycaemia in insulin-dependent diabetic subjects does not cause significant alterations in 24-h BP in either diabetic or normal subjects.

Adult↗
PubMed1994

Fasting and postprandial phenylalanine and leucine kinetics in liver cirrhosis.

To investigate body protein turnover and the pathogenesis of increased concentration of plasma phenylalanine in liver cirrhosis, we have studied phenylalanine and leucine kinetics in cirrhotic (diabetic and nondiabetic) patients, and in normal subjects, both in the postabsorptive state and during a mixed meal, using combined intravenous and oral isotope infusions. Postabsorptive phenylalanine concentration and whole body rate of appearance (Ra) were approximately 40% greater (P < 0.05) in patients than in controls. Leucine concentrations were comparable, but intracellular leucine Ra was also increased (P < 0.05), suggesting increased whole body protein breakdown. Postprandial phenylalanine Ra was also greater (P < 0.05) in the patients. This difference was due to a diminished fractional splanchnic uptake of the dietary phenylalanine (approximately 40% lower in the cirrhotics vs. controls, P < or = 0.05). Postprandial leucine Ra was also increased in the patients, but splanchnic uptake of dietary leucine was normal. Thus both increased body protein breakdown and decreased splanchnic extraction of dietary phenylalanine can account for the increased phenylalanine concentrations in liver cirrhosis.

Adult↗
PubMed1994

Effects of metformin treatment on whole-body and splanchnic amino acid turnover in mild type 2 diabetes.

The effects of metformin therapy on whole body and splanchnic amino acid turnover are not known. Therefore, we have studied fasting and postprandial phenylalanine kinetics in type 2 diabetic subjects (non-insulin-dependent diabetes mellitus), previously treated with diet only, both before and after 4 weeks of either metformin (850 mg twice a day) (n = 11) or placebo administration (n = 6). Phenylalanine kinetic was evaluated by means of a multiple isotope technique: tritiated phenylalanine was infused i.v., whereas carbon-labeled phenylalanine was incorporated into a chemically-defined meal. Compared with placebo, metformin administration decreased both fasting (from 162 +/- 17 to 141 +/- 20 mg/dl) and postprandial (from 217 +/- 20 to 164 +/- 20 mg/dl) glucose concentrations (P < 0.05-P < 0.01). Fasting insulin concentrations were unaffected, but postmeal insulin tended to be lower (P < 0.06) after metformin. Compared with the pretreatment period, metformin administration did not change total phenylalanine rate of appearance (fasted state, 0.74 +/- 0.10 vs. 0.71 +/- 0.08 mumol/kg.min; fed state, 0.77 +/- 0.10 vs. 0.75 +/- 0.08 mumol/kg.min, respectively), dietary and endogenous phenylalanine rate of appearance, dietary phenylalanine oxidation, and splanchnic uptake, similar to what was observed in the placebo group. Our data indicate that, at least after a 4-week treatment, metformin does not affect fasting and postprandial protein turnover, as indicated by phenylalanine data, in subjects with mild non-insulin-dependent diabetes mellitus.

Amino Acids↗