PubMed Health⌕ Search

Biomedical subjects

L L Levitsky

Publications and source records attributed to L L Levitsky.

At least 37 records · Page 2Linked to original sources
PubMed1988

Energy expenditure and body composition in Prader-Willi syndrome.

Patients with Prader-Willi syndrome are frequently obese. To determine if obesity is partially explained by a low energy expenditure, we compared total daily energy expenditure, basal metabolic rate, and body composition in Prader-Willi patients with obese controls. Total energy expenditure was measured by doubly labeled water, basal metabolic rate was measured by respiratory gas analysis using an open-system canopy design, and body composition was calculated from total body water determinations using 18O labeled water. In six Prader-Willi subjects, basal metabolic rates were normal when compared on the basis of fat free mass, but not body surface area or height, weight, and age. Ten Prader-Willi subjects (8 to 24 years-old) had a total daily energy expenditure (+/- SD) of 1,980 +/- 580 kcal/d, which was 47% less than their obese controls (3,700 +/- 820 kcal/d). When normalized for their smaller fat free mass and body mass, however, the difference was only 14% (P less than .01). The results indicate that the low energy expenditures in Prader-Willi syndrome are mostly due to the small fat free mass in these patients and not due to any difference in energy efficiency at the cellular level. Prader-Willi subjects who had lost weight and were at or near weights appropriate for their heights were still 30% to 40% body fat. Because this excess fat was not evident from skinfold measures, usual anthropometric measures were not reliable indicators of total body fat in these subjects.

Adipose Tissue↗
PubMed1988

Precursors to glycogen in ovine fetuses.

Postprandial hepatic glycogenesis in the adult animal is now felt to proceed largely through gluconeogenic pathways rather than directly from glucose. The ovine fetus, like the mature sheep, lacks specific hepatic glucokinase. Therefore, we examined the role of lactate as a fetal glycogenic precursor in seven chronically catheterized 125-day sheep fetuses. Fetuses were infused with L-[U-14C]lactate and D-[3-3H]glucose (50 microCi load, 50 microCi/h for 5 h), while maternal glucose was maintained at 50 mg/dl. Mean fetal hepatic glycogen specific activity (microCi/mg x 10(3] was 0.82 +/- 0.08 for 14C and 2.6 +/- 0.4 for 3H, whereas fetal renal glycogen specific activity was 0.46 +/- 0.22 for 14C and 0.78 +/- 0.16 for 3H. In contrast, [14C]glucose specific activity was undetectable in blood (limit of detectability 1 microCi/mg x 10(3] and mean [3H]glucose specific activity was 8.9 +/- 1.3 microCi/mg x 10(3]. The least detectable specific activity of [14C]glucose did not differ significantly from the [14C]glycogen enrichment in liver, whereas [3H]glucose specific activity was significantly (P less than 0.02) greater than [3H]glycogen enrichment. We conclude that glycogenesis from glucose is partly through the indirect gluconeogenic route and that lactate may be a glycogenic precursor in the ovine fetus.

Animals↗
PubMed1987

Partial androgen resistance due to a distinctive qualitative defect of the androgen receptor.

Using whole genital skin fibroblasts, we have characterized a novel androgen receptor mutation in a family with partial androgen resistance. The proposita was born with bilateral labioscrotal folds and a single perineal urogenital orifice. Her similarly affected maternal aunt was raised as a female with the support of gonadectomy and vaginoplasty. The mutant androgen receptor has a normal maximum binding capacity (Bmax), but an increased apparent equilibrium dissociation constant (Kd) with 5 alpha-dihydrotestosterone (DHT) and 2 synthetic androgens, methyltrienolone (MT) and mibolerone (MB). Preformed mutant DHT-receptor complexes dissociate (k) at a near-normal rate, but their MT and MB counterparts dissociate twice as quickly as normal. The native free mutant receptor is not more thermolabile than normal, but its recently dissociated counterpart is. Prolonged incubation of the cells with each of the 3 androgens causes the mutant receptor to acquire a normal increment of increased androgen-receptor activity. This androgen-sensitive pattern of misbehavior of the present mutant receptor distinguishes it from those responsible for 3 other families with partial androgen resistance studied previously. These differences will help to identify structure-function domains on the androgen receptor protein, particularly in conjunction with the use of DNA probes to analyze mutations at the X-linked androgen receptor locus.

Androgen-Insensitivity Syndrome↗
PubMed1986

The effect of dexamethasone and surgically induced intrauterine growth retardation on renal and hepatic levels of phosphoenolpyruvate carboxykinase in the rat.

Renal and hepatic levels of the rate-limiting gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PEPCK) were determined in control and intrauterine growth-retarded rate neonates and dams. Dexamethasone and surgically induced intrauterine growth retardation (IUGR) resulted in an elevation of neonatal renal PEPCK activity, but did not affect hepatic PEPCK levels. In the dam, glucocorticoid administration resulted in an increase in renal PEPCK, but did not affect the hepatic enzyme. We have demonstrated that, unlike the hepatic enzyme, renal PEPCK could potentially contribute to gluconeogenesis in utero, since dexamethasone administration significantly increased renal PEPCK at birth. This study confirms the hypothesis that hepatic and renal PEPCK activities are regulated independently in both the adult and neonatal animal.

Animals↗
PubMed1986

Gluconeogenesis from lactate in the chronically catheterized baboon fetus.

Gluconeogenesis from lactate may be qualitatively identified in the chronically catheterized baboon fetus in the maternal fed and fasted state. Infusion of 250 microCi U-14C-lactate to the fetus over a 150-min period leads to the appearance of 14C-glucose in the fetal circulation. Little 14C-lactate or glucose appears in the maternal circulation, supporting fetal production of glucose from lactate. Maternal glucose infusion seems to inhibit fetal gluconeogenesis. The mean plateau in percent disintegrations per minute of glucose compared to lactate in the maternal fed state is 14.7 +/- 2.2 compared to 16.1 +/- 3.0 in the maternal fasting state and 11.1 +/- 0.6 during maternal glucose infusion. It is clear that the primate fetus is capable of gluconeogenesis before term. Quantitation of this capacity awaits development of a model permitting assessment of maternal-placental and fetal substrate flux.

Animals↗
PubMed1984

Splanchnic uptake and release of energy substrates in the fasting baboon infant.

Estimates of splanchnic energy substrate exchange in the primate infant have been obtained using a baboon model. The splanchnic bed of the fasting baboon newborn released glucose at an estimated rate of 14.5 +/- 5.0 mumol/min X kg body weight. Splanchnic glucose release in the fasting 5-7 wk old baboon infant proceeded similarly at an estimated rate of 15.5 +/- 4.5 mumol/min X kg body weight. The principal precursors taken up by the splanchnic bed were lactate, glycerol, and alanine. Uptake of alanine correlated in a linear fashion with glucose release. Lactate was the most important precursor in both age groups. Glucose recycling through lactate is an active mechanism in the primate fetus as well as in the young of other species.

Alanine↗
PubMed1982

Prepubertal gynecomastia associated with estrogen-containing hair cream.

Gynecomastia associated with high plasma estrogen levels was observed in a prepubertal boy. The family initially denied ingestion or application of any medications despite careful review of the history, but endocrinologic findings were not consistent with endogenous estrogen production. Persistent inquiry discovered the use of a hair cream containing substantial amounts of estrogen. After discontinuation of its use, breast tissue regressed and estrogen levels returned to normal. To our knowledge, scalp inunction has not hitherto been reported as a cause of prepubertal gynecomastia.

Child, Preschool↗
PubMed1982

Echocardiographic evidence for impaired myocardial performance in children with type I diabetes mellitus.

Thirty-three children with type I diabetes mellitus and 51 normal children underwent M-mode echocardiography. Abnormalities of myocardial performance were present in many of the diabetic children. The mean end-systolic volume of the left ventricle was greater in diabetics compared to control subjects. Mean ejection fraction, minor axis shortening, and velocity of circumferential fiber shortening were decreased in the diabetics. There was no evidence of increased myocardial mass in these diabetic children. There was no correlation between myocardial dysfunction, clinical assessment of control, or glycohemoglobin in the diabetic children.

Adolescent↗
PubMed1981

HLA types in American black juvenile diabetics strong associations with Dw3 and Dw4.

The distributions of HLA-A, -B, -C and -D antigens in 38 black American insulin-dependent juvenile diabetics were studied. Antigens A1, A2, B8 and Cw3 were slightly increased, but the corrected probability values were not statistically significant. As determined by mixed lymphocyte culture, the frequency of Dw3 was 89% in the juvenile diabetics and that of Dw4 was 42% in comparison with 14 and 8%, respectively, in the controls. The relative risks for juvenile diabetes were 52 for Dw3 (p = 10(-8) and 9 for Dw4 (p = 10(-6). Dw2 was significantly decreased in the diabetics (p equals 0.008). All of these deviations in A, B, C and D locus specificities have been previously reported by others in white juvenile diabetics. Because there are white genes in the American black gene pool and juvenile diabetes is rare in blacks in western Africa, many cases of juvenile diabetes in American blacks could be the result of genes ultimately derived from the white genes. This hypothesis is supported by the similar HLA associations in juvenile diabetes in the black and white ethnic groups.

Black People↗
PubMed1981

Uptake and release of energy substrates, oxygen, and carbon dioxide by the hindlimb of the fasting infant baboon.

Veno-arterial differences for energy substrates across hindlimb tissues were measured in baboon infants at birth and at 6 weeks. Hindlimb glucose uptake was 2.36 +/- 0.80 microM/min in the newly born baboons and 1.81 +/- 0.56 microM/min in the 6-week-old infants. The major precursor release by the infant baboon hindlimb was lactate, although release of alanine and glycerol was significant. These studies complement previous data suggesting that glycolysis is a major pathway for energy production in the infant primate.

Animals↗
PubMed1980

Arterial blood levels of energy substrates and evidence for renal glucose production in the baboon infant.

The age-related changes in fasting arterial levels of energy substrates and insulin were studied at birth and/or 6 wk in eleven baboon infants. In addition, the renal contribution to glucose release in the primate infant was estimated. Arterial blood glucose levels were similar in six fasted newborns and in nine fasted 6-wk-old infants. Arterial blood lactate, alanine, pyruvate, glutamate, and glutamine levels were significantly higher (P < 0.01) in the new born animals, and beta-hydroxybutyrate was significantly higher in the older animals (P < 0.001). Arterial plasma insulin levels were low in both groups. Levels of blood glucose in the inferior vena cava below the renal vein were significantly lower than levels in the aorta (P < 0.01). In contrast, levels of blood glucose in the inferior vena cava above the renal vein were significantly higher than in the aorta (P < 0.05). Computed renal vein glucose levels were higher than those in the aorta (P < 0.01). In the newborn infants, there was significant renal uptake of lactate, pyruvate, glycerol, and glutamine (P < 0.01), and release of beta-hydroxybutyrate (P < 0.05). In the older animals, there was renal uptake of alanine, lactate, pyruvate, and glycerol (P 0.01). Mean cardiac output per kg body weight did not differ significantly in the newborn and 6-wk-old infants. Lactate uptake was potentially responsible for 59% of mean renal glucose output in the newborn and 76% of mean renal glucose output in the older infant. Net renal glucose release in eight 6-wk-old infants was estimated to be 3.5 +/- 1.1 microM/min . kg (95% confidence limits, 0.7 < 3.5 < 6.2). Net renal glucose release in three newborn infants was 4.7, 5.4, and 19.8 microM/min . kg. There was a significant linear relationship between arterial lactate levels and renal glucose production in the older infants (P < 0.05). Extremely low arterial pH was associated with increased renal glucose release in the newborn, and high arterial pH with decreased or absent glucose release in the 6-wk-old animals.

Age Factors↗