Biomedical subjects

K L Minaker

Publications and source records attributed to K L Minaker.

At least 55 records · Page 3Linked to original sources

PubMed1989

Phenytoin-induced improvement in muscle cramping and insulin action in three patients with the syndrome of insulin resistance, acanthosis nigricans, and acral hypertrophy.

Phenytoin sodium has been used to treat muscle cramps of diverse causes, and is known to increase insulin sensitivity during long-term use. We have previously described a syndrome of insulin resistance, acanthosis nigricans, and acral hypertrophy with continual muscle cramping. The effect of 300 mg/d of phenytoin (Dilantin) on muscle cramping and carbohydrate economy was studied in three affected patients and four control subjects. Oral glucose tolerance tests, euglycemic insulin infusion studies, and monocyte insulin binding tests were conducted before and after phenytoin administration. All three patients had notable improvement in muscle cramps. In response to phenytoin, metabolic improvements were variable, with improvement characteristically better in patients with less severe baseline metabolic abnormalities. Patient 1, with the mildest degree of glucose intolerance, had decreased fasting insulin and blood glucose levels, improved glucose tolerance, and insulin-mediated glucose disposal, associated with an increase in monocyte insulin receptors. Patient 2 had reduced fasting plasma glucose and insulin levels and improved oral glucose tolerance, suggesting a beneficial effect on carbohydrate metabolism. Patient 3, with the most severely impaired carbohydrate economy, showed no metabolic improvement despite marked lessening of muscle pain. These clinical characteristics were unaffected in control subjects. We conclude that phenytoin is of value in the therapy of muscle cramps and glucose intolerance in patients with this syndrome.

Acanthosis Nigricans↗

PubMed1989

Effect of insulin on plasma norepinephrine and 3,4-dihydroxyphenylalanine in obese men.

Increasing evidence relates serum insulin level and blood pressure in obese individuals. Although the connection between these two factors is not established, a common presumption is that the sympathetic nervous system is somehow involved, in part, because laboratory studies demonstrate insulin stimulation of sympathetic and cardiovascular activity. Because the obese may exhibit altered responsiveness to insulin action, the current investigation compared cardiovascular and neurohumoral responses to euglycemic insulin infusion (200 mU/m2/min) in obese and lean men. At baseline, obese men displayed higher glucose and insulin levels, faster pulse rates, and elevated mean arterial pressures (MAP) than lean controls; plasma norepinephrine (NE) and 3,4-dihydroxyphenylalanine (DOPA) concentrations, however, did not differ. During insulin infusion, pulse rate increased equally in obese and lean subjects (from 69 to 78 min-1 in obese and from 56 to 66 min-1 in lean subjects), while MAP remained unchanged in both groups. Elevations in plasma NE (+85 pg/mL in obese and +109 in lean pg/mL) and reductions in plasma DOPA (-233 pg/mL in obese and -376 pg/mL in lean) did not differ between groups. Sodium excretory rate decreased during insulin infusion in lean subjects by 2.2 mEq/h but increased in obese by 5.3 mEq/h (difference in response between groups, P = .024). Thus, in these obese men, cardiovascular and sympathetic responses to insulin persist despite evidence of moderate insulin resistance; increased sympathetic activity, as a cause for the resting tachycardia and borderline hypertension at baseline, seems unlikely.

Adult↗

PubMed1989

Leucine metabolism in aging humans: effect of insulin and substrate availability.

To elucidate the relative roles of insulin (I) and amino acid (AA) availability on body protein economy and AA kinetics, we compared whole body leucine kinetic responses, using a 360-min constant infusion of L-[1-13C]leucine, during administration of an L-AA solution to six healthy young (21-25 yr) and six healthy old (72-87 yr) men (study 1) to those when the AA solution was given in conjunction with a euglycemic I clamp (study 2). In study 1, serum I increased significantly (P less than 0.02) by 4 +/- 1 and 4 +/- 2 microU/ml in young (Y) and old (O) men, respectively. In study 2, I was raised to 91 +/- 7 (Y) and 88 +/- 7 (O) microU/ml; the glucose infusion to maintain euglycemia in the Y was significantly greater than in the O (8.0 +/- 0.1 vs. 6.8 +/- 1.9 mg.kg-1.min-1). Leucine flux and oxidation increased significantly in both age groups during the administration of AA. Estimates of leucine released from protein breakdown declined (P less than 0.01) by 18 and 20% in study 1 and 2, respectively, in the young and by 12 and 44%, respectively, in the elderly. Rates of leucine incorporation into protein increased (P less than 0.01) similarly in both age groups and in both studies. These findings emphasize the importance of AA availability in the stimulation of protein synthesis and suggest that insulin's major role in vivo is to repress whole body proteolysis. Furthermore, despite evidence of an age-related decline in glucose disposal, the elderly had similar leucine kinetic responses to hyperaminoacidemia.

Adult↗

PubMed1989

Escape of hepatic glucose production during hyperglycemic clamp.

The role of the pattern of insulin secretion on hepatic glucose production (HGP) was evaluated with hyperglycemic and euglycemic clamp studies in six normal young nonobese subjects. In the hyperglycemic studies, glucose levels were raised and maintained at 98 mg/dl above basal for 150 min. Each subject responded with a biphasic pattern of immunoreactive insulin (IRI) release. HGP was completely suppressed by 20 min, coincident with the first-phase insulin release. HGP then rose steadily, surpassing the basal rate by 100 min when IRI had reached the peak levels of the first phase. By 130 min, when IRI had surpassed the peak first-phase levels, HGP began to fall. In the euglycemic studies with a square wave of hyperinsulinemia (approximately 25 microU/ml), HGP was suppressed to approximately 60% of basal and remained at that rate. We next repeated the hyperglycemic studies with somatostatin, glucagon, and insulin infusions. In these studies with a square wave of hyperinsulinemia (approximately 40 microU/ml, the level observed during the first phase IRI of the previous hyperglycemic clamps), HGP was suppressed to approximately 43% of basal rate and remained at that rate. These studies indicate insulin regulation of HGP is not only dependent on insulin level but may be strongly influenced by the pattern, over time, of insulin secretion.

Adult↗

PubMed1989

Impairment of noninsulin-mediated glucose disposal in the elderly.

While normal aging is characterized by resistance to insulin-mediated glucose disposal (IMGU), the effect of age on noninsulin-mediated glucose disposal (NIMGU), which is responsible for the majority of basal glucose uptake, has not been completely evaluated. These studies were conducted on healthy nonobese young (n = 10; age, 20-30 yr) and old (n = 10; age, 62-80 yr) men. Each subject underwent two paired studies in random order. In all studies a [3H]glucose infusion was used to measure glucose uptake and production rates, and somatostatin (500 micrograms/h) was infused to suppress endogenous insulin release. In study A, plasma glucose was kept close to fasting levels (approximately 5.6 mmol/L) using an euglycemic clamp protocol for 4 h. Plasma insulin decreased to less than 20 pmol/L within 15 min and remained suppressed thereafter in all studies. Steady state (15-240 min) plasma glucagon levels were slightly greater in the elderly [young, 86 +/- 5 (+/- SE); old, 98 +/- 2 ng/L; P less than .05]. Basal glucose uptake was similar in both groups (young, 877 +/- 21; old, 901 +/- 24 mumol/min). Glucose uptake during the last hour of the study (180-240 min) was used to represent NIMGU, because insulin action was assumed to be absent by this time. NIMGU was less in the elderly (young, 744 +/- 18; old, 632 +/- 32 mumol/min; P less than 0.01). In study B, plasma glucose was kept at about 11 mmol/L for 4 h using a hyperglycemic clamp protocol. Plasma insulin decreased to less than 20 pmol/L within 15 min and remained suppressed thereafter in all studies. Steady state plasma glucagon levels were slightly but not significantly higher in the elderly (young, 88 +/- 6; old, 100 +/- 4 ng/L). Basal glucose uptake (young, 910 +/- 27; old, 883 +/- 25 mumol/min) and NIMGU (young, 933 +/- 36; old, 890 +/- 16 mumol/min; P = NS) were similar in both young and old subjects. We conclude that aging is associated with impairment in NIMGU only in the basal state, which may explain in part the increase in fasting glucose with age.

Adult↗

PubMed1989

Effect of age on systemic delivery of oral glucose in men.

This study examined the effect of age on the posthepatic delivery of oral glucose (PHDG) during steady-state conditions. We used an intravenous-oral modification of the euglycemic insulin-clamp technique to assess PHDG in six men aged 24-39 yr (young) and eight men aged 65-83 yr (old). Each subject underwent two studies in which insulin was infused at 120 mU.m-2.min-1 for 3 h, and either oral glucose (45 g) or water was given 60 min after initiating insulin. This level of insulin infusion is known to fully suppress hepatic glucose output. For each subject, PHDG was calculated as the difference between the whole-body glucose disposal rates in the paired studies. The time course of PHDG differed in the two groups (P less than .0001), with an overall delay in PHDG in the older men. During the 1st h, younger men showed a greater PHDG (58.6 +/- 3.8% of the oral load vs. 45.1 +/- 4.2%) than the older group (P = .04). During the 2nd h, PHDG was less in the younger group (20.7 +/- 4.9%) than the older group (36.6 +/- 3.9%, P = .02). Over the 2-h period, total PHDG was comparable in younger (79.3 +/- 7.4%) and older (81.7 +/- 7.9%) men. These results indicate that normal aging is associated with significantly delayed but overall equal PHDG in men, consistent with the greater effect of age on 2-h rather than earlier postprandial glucose levels. It reinforces the role of impaired peripheral utilization as the primary mechanism of the glucose intolerance of aging.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

Insulin-mediated hypokalemia and paralysis in familial hypokalemic periodic paralysis.

To elucidate a potential role for insulin-mediated extra-renal potassium disposal in the clinical syndrome of hypokalemic periodic paralysis, an obese affected man was studied using the euglycemic insulin clamp, which, in normal and obese subjects, produces predictable, insulin dose-dependent declines in plasma potassium levels. During a 20 mU/m2/minute euglycemic clamp (insulin level, 88 microU/ml) procedure, while the patient with hypokalemic periodic paralysis demonstrated severe resistance to insulin-mediated glucose uptake (glucose uptake 50 percent of that of normal control subjects, n = 17), his plasma potassium declined to a degree similar to that seen in normal subjects. During a subsequent higher dose, 200 mU/m2/minute insulin infusion (insulin level, 914 microU/ml), plasma potassium declined to 2.5 meq/liter, a value significantly below that seen in normal (n = 19) (3.3 +/- 0.1 meq/liter) and obese (n = 6) (3.2 +/- 0.1 meq/liter) subjects. During this study, paralysis began in the patient's hand and forearm at the potassium nadir and lasted three hours, despite restoration of normokalemia 30 minutes after paralysis began. Glucose disposal rates during this high-dose insulin infusion were one-half that seen in lean control subjects (n = 19) and similar to those in obese control subjects. If these findings are representative of hypokalemic periodic paralysis and can be generalized to larger numbers of patients, they indicate several new features of this syndrome. The ability of insulin to induce hypokalemia is enhanced in this syndrome even in the presence of marked coexistent obesity-related resistance to the action of insulin to promote glucose utilization. Enhanced sensitivity of potassium uptake systems to activation by insulin (and other factors) may be a central feature of this syndrome. Additionally, paralytic hypokalemia can be induced during a euglycemic insulin clamp procedure, which could be utilized as a diagnostic test for this syndrome.

Adult↗

PubMed1988

Somatostatin infusion enhances hepatic glucose production during hyperglucagonemia.

Somatostatin (SRIH) is widely employed in metabolic studies to permit quantitation of glucose production and disposal rates while the endocrine pancreas is suppressed and the hormonal milieu is under the investigator's control. In these studies it is assumed that if peripheral levels of insulin and glucagon are the same during SRIH infusion as during control studies, the effects of these hormones on glucose metabolism are equivalent. If the effect of glucagon is influenced by SRIH infusion, then these techniques may be unsuitable for the study of the regulation of hepatic glucose output. To assess the influence of SRIH on glucagon-stimulated hepatic glucose production (Ra), we determined Ra during paired studies in ten healthy (five younger and five older) subjects. In each study an insulin infusion designed to yield physiologic systemic insulin levels of 20 to 30 microU/mL was given from 0 to 210 minutes. In addition, from 60 to 210 minutes either glucagon alone (3.5 ng/kg/min) (I + IRG) or glucagon (3.5 ng/kg/min) and SRIH (250 micrograms/h) (I + IRG + SRIH) was infused. Since results for plasma levels of insulin, C-peptide, glucagon, and Ra were similar in young and old subjects, the two age groups were combined for analysis. Basal plasma insulin, glucagon, C-peptide, glucose, and Ra were similar in each arm of the study. Insulin values were nearly identical from 60 to 210 minutes (I + IRG, 23.8 +/- 1.1; I + IRG + SRIH, 24.0 +/- 1.0 microU/mL).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

Glucose and amino acid metabolism in aging man: differential effects of insulin.

Insulin is a major regulator of glucose and body protein homeostasis, both of which demonstrate age-related changes. To clarify insulin's role in these age-related changes and to compare age-related glucose and protein homeostatic responses, insulin-mediated aspects of glucose and amino acid metabolism were simultaneously examined in healthy postabsorptive young (n = 5, mean age, 25 years) and elderly (n = 5, mean age, 76 years) men. Primed constant infusions of L-[1-13C]leucine and L-[15N]alanine were administered during a basal period (0 to 180 minutes) and during four separate single rate euglycemic insulin infusions (180 to 360 minutes). Steady state insulin concentrations were 16 +/- 1, 29 +/- 3, 75 +/- 5, and 2407 +/- 56 microU/mL in the young and 23 +/- 4, 37 +/- 8, 96 +/- 11 and 3,357 +/- 249 microU/mL in the elderly at the different insulin infusion rates of 6, 10, 30, and 400 mU mU.m-2.min-1, respectively. For the 6 and 10 mU insulin infusion rates, a primed, constant infusion of [6,6 - 2H2]glucose permitted quantitation of hepatic glucose production. Glucose disposal rates adjusted for lean body mass (LBM) were lower in the elderly than in the young at the 6, 10, and 30 mU insulin infusion rates and similar in the two age groups in the 400 mU studies. Insulin dose-dependent reductions occurred in eight of ten plasma amino acids and were not influenced by age. There was an insulin dose-dependent reduction in plasma leucine flux which was similar in both age groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

Somatostatin enhances insulin-mediated glucose disposal in elderly subjects.

Somatostatin (SRIH) infusion has been widely used in metabolic studies of carbohydrate metabolism. While the effects of SRIH itself on various aspects of carbohydrate economy have been assessed in young adults, such studies have not been conducted in the elderly, which represent an increasingly important study group. To examine the effect of SRIH on insulin-mediated glucose disposal in the elderly, we studied 12 (7 men and 5 women) healthy nonobese subjects, aged 65-80 yr. Paired 3-h euglycemic insulin clamp studies were performed in random order employing insulin alone (22 mU/m2.min) or insulin with SRIH (250 micrograms/h) and glucagon (0.4 ng/kg.min) to maintain normal basal plasma glucagon levels. Basal plasma insulin, glucose, glucagon, GH, and glucose production and disappearance were similar on each occasion. Steady state (10-180 min) mean plasma insulin [insulin alone, 298 +/- 12 (+/- SE); insulin; glucagon, and SRIH, 304 +/- 15 pmol/L] and glucagon (insulin alone, 85 +/- 7; insulin, glucagon, and SRIH, 96 +/- 9 ng/L) concentrations were similar. At steady state (150-180 min) glucose production was suppressed to similar levels (insulin alone, 26 +/- 7; insulin, glucagon, and SRIH, 36 +/- 13 mumol/kg.min). However, steady state glucose disposal was significantly higher during the SRIH infusion (insulin alone, 295 +/- 26; insulin, glucagon, and SRIH, 346 +/- 32 mumol/kg.min; P less than 0.02). We conclude that SRIH augments insulin-mediated glucose disposal in healthy older subjects at physiological levels of insulin.

Age Factors↗

PubMed1987

Aging and diabetes mellitus as risk factors for vascular disease.

During this century, cardiovascular diseases have become the major cause of death for elderly and diabetic patients. Although risk factors for vascular diseases have been identified, the interactions of aging and diabetes on the prevalence and incidence of vascular disease have not been systematically studied. A spectrum of such interactions appears to exist. Future research efforts are likely to permit accurate weighting of the influence that diabetes and aging have on vascular disease.

Adult↗

PubMed1987

Plasma tryptophan and total neutral amino acid levels in men: influence of hyperinsulinemia and age.

Because of the well-recognized age-related changes in peripheral tissue sensitivity to insulin and the demonstrated impact of insulin on blood amino acid profiles in young individuals, we evaluated the influence of insulin level and age on the concentrations of tryptophan and its ratio to the sum of the large neutral amino acids (LNAA). The ratio of the plasma concentrations of tryptophan and the LNAA (leucine, isoleucine, valine, tyrosine, and phenylalanine), may be an important determinant of the rate at which tissues synthesize neurotransmitters, such as catecholamines and serotonin. Each of five healthy young (21 to 34 yr) and five healthy old subjects (67 to 85 yr) received, on separate occasions, euglycemic insulin infusions at rates of 6, 10, 30, and 400 mU X m-2 X min-1. Basal plasma tryptophan concentrations and LNAA levels were similar in young and old. Both tryptophan and LNAA levels decreased in an insulin dose-dependent manner (P less than .02). The dose-response effect of insulin on tryptophan levels in the elderly was less than in the young (P less than .03), while the response of the LNAA was similar in both age groups. The ratio of tryptophan to LNAA was less in the old when compared to the young (P less than .03) but increased in the two age groups in an insulin-dose-dependent fashion (P less than .02). Maximal plasma tryptophan decrements were 39% and 32%, and maximal LNAA declines were 58% and 61% in young and old, respectively, during the 400 mU X m-2 X min-1 studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1987

Insulin action in aging man: evidence for tissue-specific differences at low physiologic insulin levels.

This study examined the effect of age on insulin action in several tissues. Euglycemic insulin clamp studies were performed on healthy young (n = 7, 20 to 35 years, 10 and 20 mU/m2 X min insulin infusions) and old (n = 7, 66 to 80 years, 8 and 16 mU/m2 X min insulin infusions) adults. Insulin values were similar during both the lower (young, 24 +/- 1.6, old, 24 +/- 2.1 microU/ml) and higher (young, 40 +/- 3.3; old, 39 +/- 3.8 microU/ml) insulin infusion rates. Although suppression of hepatic glucose output (HGO) was more rapid (p less than .05) in the elderly group at each dose, HGO was eventually suppressed to similar levels in both age groups (low dose: young, 34.4 +/- 10.8, old, 25.3 +/- 1.8 mg/m2 X min; higher dose: young, 22.8 +/- 10.2, old, 6.2 +/- 2.1 mg/m2 X min). Glucose disposal was less (p less than .01) in the aged group at both insulin infusion rates. Suppression of C-peptide was slower in the elderly participants (p less than .05) in the low dose study. Suppression of free fatty acid and glucagon levels was the same in each age group. We concluded that the insulin resistance of aging is not generalized to all tissues.

Adult↗

PubMed1987

Somatostatin does not alter insulin-mediated glucose disposal.

We examined the effect of somatostatin (SRIH) infusion on insulin-mediated glucose disposal (Rd) in normal young subjects (n = 8) to determine the influence of SRIH on insulin action. Paired 3-h euglycemic insulin clamp studies were performed in random order employing insulin alone (25 mU/m2 X min) or insulin with SRIH (250 micrograms/h) and replacement of basal glucagon (0.4 ng/kg X min). Basal plasma glucose, insulin, glucagon (IRG), and GH concentrations, hepatic glucose production, and Rd were similar on each occasion. Steady state (10-180 min) plasma insulin insulin alone, 283 +/- 10 (+/- SEM); insulin, IRG, and SRIH, 284 +/- 10 pmol/L) and glucagon levels (insulin alone, 84 +/- 7; insulin, IRG, and SRIH, 82 +/- 7 ng/L) were similar. Hepatic glucose production (insulin alone, 0.66 +/- 0.12; insulin, IRG, and SRIH, 0.78 +/- 0.48 mg/kg X min) and Rd (insulin alone, 8.16 +/- 0.62; insulin, IRG, and SRIH, 8.17 +/- 0.61 mg/kg X min) were not different at steady state. We conclude that SRIH infusion with glucagon replacement does not augment insulin-mediated glucose disposal in normal young subjects at physiological insulin levels.

Adult↗

PubMed1986

Cardiovascular and norepinephrine responses after meal consumption in elderly (older than 75 years) persons with postprandial hypotension and syncope.

Aging is associated with alterations in cardiovascular homeostasis that impair adaptation to common hypotensive stresses. Postprandial blood pressure (BP) reduction has been described in elderly subjects, but its clinical significance and pathophysiologic mechanisms are unknown. We have identified 8 elderly patients with meal-related syncope and large postprandial BP declines. To evaluate the role of sympathetic nervous system activity and insulin in the development of postprandial BP reduction, mean arterial BP, heart rate, plasma catecholamine and insulin responses to a high carbohydrate meal in these 8 syncope patients were compared with those of 7 young and 12 old nonsyncopal controls. By 60 minutes after the meal, mean arterial BP declined an average of 26 mm Hg (p = 0.001) in old syncope patients, in contrast to a decline of 9 mm Hg (p = 0.1) in elderly controls and no change in young controls. Young and old controls had significant, sustained increases in heart rate or plasma norepinephrine levels, or both, throughout the 90-minute postprandial period. However, elderly syncope patients had no significant change in heart rate and only an initial increase but subsequent sustained decrease in plasma norepinephrine levels that paralleled the marked mean arterial BP reduction. Insulin and glucose responses were not significantly correlated with mean arterial BP reduction. These findings demonstrate that compared with old and young controls, elderly patients with meal-related syncope have marked sustained declines in postprandial mean arterial BP associated with a failure to maintain compensatory norepinephrine levels and cardioacceleratory responses.

Aged↗

PubMed1986

Splanchnic factors enhance the norepinephrine response to oral glucose in aged man.

Oral glucose has been shown to increase sympathetic nervous system (SNS) activity more in old than in young subjects. In contrast intravenous glucose during euglycemic hyperinsulinemia increases SNS activity in young but not in old subjects. To evaluate the role of splanchnic factors in this discrepancy, we employed a modification of the glucose clamp technique in 6 young (24-39 years) and 8 old (65-83 years) normal males. Each subject underwent two studies in which insulin was infused at 120 mU/m2 X min for 3 h and either oral glucose (50 gms) or water was given 60 min after initiating insulin. Euglycemia was maintained in all studies. When compared to control drink, oral glucose elevated norepinephrine in old (p less than 0.01), but not in young subjects. The difference between old and young was significant (p less than 0.02). When compared to control drink, oral glucose increased pulse rate and double product in the young, and pulse rate in the old. These results indicate that oral glucose activates the SNS in the elderly via splanchnic mechanisms independent of changes in circulating levels of glucose or insulin.

Administration, Oral↗

PubMed1986

Insulin resistance and regulation of serum amino acid levels in myotonic dystrophy.

To quantify the degree of whole body insulin resistance in patients with myotonic dystrophy and to determine if these same patients display signs of a whole body decrease in the action of insulin on amino acid uptake and glucose disposal, three separate 120 min studies employing the euglycaemic insulin clamp technique (20, 80 and 200 m-units min-1 m-2) were performed on five ambulatory patients with myotonic dystrophy. The results were compared with findings obtained in identical studies in 21 normal volunteers. Myotonic dystrophy patients showed a slower, less marked decline in the serum concentration of insulin sensitive amino acids (threonine, valine, leucine, isoleucine, tyrosine, phenylalanine) during all three insulin infusions compared with normals. The greatest difference occurred at the low physiological elevations of insulin produced by the 20 m-units min-1 m-2 infusion. Alanine levels fell significantly below baseline in patients with myotonic dystrophy after 60 and 120 min of insulin infusion with all three rates of insulin infusion. Normal subjects had only a minimal, insignificant decline in arterialized alanine concentrations during the three different insulin infusions. Creatinine adjusted rates of whole body glucose disposal were 30-40% lower in the myotonic dystrophy group at all three doses of insulin compared with the normals. This demonstrates that their insulin resistance was not due simply to a reduction in muscle mass. The overall pattern of findings in these studies of patients with myotonic dystrophy indicates that there is a whole body derangement in the regulation of circulating amino acid levels by insulin as well as a marked decrease in the action of this hormone in stimulating glucose uptake by target tissues.

Adult↗

PubMed1986

Insulin dose-dependent reductions in plasma amino acids in man.

The quantitative relationship between insulin and plasma amino acid (AA) levels were characterized in five healthy young men during euglycemic insulin infusions (6, 10, 30, and 400 mU . m-2 . min-1). The endogenous production and disposal of glucose were determined for the 6 mU . m-2 . min-1 insulin infusion using 6,6-dideuteroglucose. While 8 of 10 AA decreased in a dose-responsive pattern to increasing levels of insulin, alanine and glycine concentrations remained unaffected. For isoleucine and proline, the insulin levels required for a half-maximal response were less than for glucose disposal (P less than 0.05), but, for all other insulin-influenced AA, the levels required were similar to those for glucose disposal. These studies indicate that insulin sensitivity of AA is similar to that of glucose disposal and that AA responses to insulin exhibit a physiologically relevant, dose-response relationship.

Adult↗