Relationship of maternal protein turnover and lean body mass during pregnancy and birth length

2001 ◽  
Vol 101 (1) ◽  
pp. 65 ◽  
Author(s):  
Sarah L. DUGGLEBY ◽  
Alan A. JACKSON
Keyword(s):  
Lean Body Mass ◽  
Body Mass ◽  
Protein Turnover ◽  
Birth Length ◽  
Relationship Of ◽  
Pregnancy And Birth

Relationship of maternal protein turnover and lean body mass during pregnancy and birth length

2001 ◽  
Vol 101 (1) ◽  
pp. 65-72 ◽  
Author(s):  
Sarah L. DUGGLEBY ◽  
Alan A. JACKSON
Keyword(s):  
Body Composition ◽  
Lean Body Mass ◽  
Body Mass ◽  
Protein Turnover ◽  
Adult Life ◽  
Birth Length ◽  
Whole Body ◽  
Body Protein ◽  
Increased Risk ◽  
Size At Birth

Epidemiological evidence shows that small size at birth is associated with an increased risk of developing cardiovascular and metabolic disease in adult life. We have examined the relationships between size at birth and maternal body composition and protein turnover in normal pregnant women. A group of 27 multiparous Caucasian women with singleton pregnancies were studied at around 18 and 28 weeks' gestation. Body composition was determined by anthropometry, and whole-body protein turnover was estimated by using a single oral dose of [15N]glycine and the end-product method. The baby's weight and length were measured within 48 h of birth. Mothers with a greater lean body mass had higher rates of protein turnover at 18 weeks' gestation. This association was largely accounted for by differences in the mother's visceral, rather than muscle, mass. Mothers who had higher protein turnover at 18 weeks' gestation had babies that were longer at birth. After adjustment for the duration of gestation and the baby's sex, 26% of the variation in length at birth was accounted for by maternal protein synthesis at 18 weeks' gestation. Maternal protein intake was not associated with the baby's birth length. Thus the mother's ability to nourish her fetus is influenced by her body composition and her rate of protein turnover. Dietary intake does not adequately characterize this ability.

Relationship of anthropometric dimensions to lean body mass in children

1978 ◽  
Vol 5 (5) ◽  
pp. 469-482 ◽  
Author(s):  
M.H. Slaughter ◽  
T.G. Lohman ◽  
R.A. Boileau
Keyword(s):  
Lean Body Mass ◽  
Body Mass ◽  
Relationship Of

scholarly journals Insights into the Abnormalities of Chronic Renal Disease Attributed to Malnutrition

2002 ◽  
Vol 13 (suppl 1) ◽  
pp. S22-S27
Author(s):  
William E. Mitch
Keyword(s):  
Lean Body Mass ◽  
Body Mass ◽  
Protein Turnover ◽  
Serum Proteins ◽  
Chronic Renal Disease ◽  
Protein Levels ◽  
Proteolytic Pathway ◽  
Ubiquitin Proteasome ◽  
Proteasome Pathway ◽  
Biochemical Mechanisms

ABSTRACT. Low values of serum proteins and loss of lean body mass are commonly found in patients with chronic renal insufficiency (CRI) and especially in dialysis patients. These abnormalities have been attributed to malnutrition (i.e., an inadequate diet), but available evidence indicates that this is not the principal cause. In contrast, there is persuasive evidence that secondary factors associated with the CRI condition cause abnormalities in protein turnover and ultimately result in low serum protein levels and loss of lean body mass. Recent reports have identified some factors that could interfere with the control of protein turnover in CRI patients, including acidosis, inflammation, and/or resistance to anabolic hormones. Each of these stimulates protein breakdown in muscle and activates a common proteolytic pathway, the ubiquitin-proteasome pathway. Moreover, acidosis or inflammation suppress hepatic albumin synthesis. Understanding the biochemical mechanisms that regulate the ubiquitin-proteasome and other catabolic pathways are required to identify new strategies for preventing protein deficits that are associated with CRI.

Relationship of red cell mass and energy metabolism to lean body mass in hypophysectomized rats

1970 ◽  
Vol 29 (1) ◽  
pp. 10-12 ◽  
Author(s):  
C. E. Bozzini ◽  
J. A. Kofoed ◽  
H. F. Niotti ◽  
R. M. Alippi ◽  
J. A. Barrionuevo
Keyword(s):  
Energy Metabolism ◽  
Lean Body Mass ◽  
Body Mass ◽  
Cell Mass ◽  
Red Cell ◽  
Red Cell Mass ◽  
Hypophysectomized Rats ◽  
Relationship Of

Exploring the relationship of self-reported lack of appetite to patient characteristics and symptom burden.

2017 ◽  
Vol 35 (31_suppl) ◽  
pp. 187-187
Author(s):  
Kelly Hyland ◽  
Alyssa L Fenech ◽  
Diane Portman ◽  
Kristine A. Donovan
Keyword(s):  
Palliative Care ◽  
Body Weight ◽  
Lean Body Mass ◽  
Body Mass ◽  
Early Identification ◽  
Symptom Burden ◽  
Patient Characteristics ◽  
Care Clinic ◽  
Relationship Of ◽  
The Relationship

187 Background: Cancer anorexia-cachexia syndrome (CACS) in patients is associated with decreases in lean body mass and body weight. Self-reported lack of appetite may be an important indicator for early identification of CACS. The current analyses examined the relationship of perceived lack of appetite to patient characteristics and overall symptom burden in a large mixed cancer sample referred to a palliative care clinic. Methods: We conducted a retrospective review of patients newly referred to an outpatient palliative care clinic over a two-year period. Data on demographic and clinical characteristics and patient-reported symptom scores on the Edmonton Symptom Assessment Scale (ESAS) were abstracted. Pearson’s correlations and ANOVAs were used to assess relationships between variables. Multiple regression analysis was used to evaluate the relative contribution of variables that were significantly correlated with lack of appetite at the univariate level. Results: Data on 544 patients ( M=53.7 years) showed that older age (r=12, p<.01), not being married or in a marriage-like relationship (r=.09, p=.04), having insurance other than managed care insurance (r=.10, p=.02), lower body mass index (BMI; r=.11, p<.01), marijuana use (r=.18, p<.0001), and overall symptom burden (ESAS total score r=.52, p < .0001) were associated with worse lack of appetite ( M=3.5, SD=3.1). Patients who were underweight (BMI <18.5, 46.7%) reported significantly worse lack of appetite than patients who were normal weight, overweight, or obese ( M=3.9, SD=3.2, p<.01). The final hierarchical regression model accounted for 34% of the variance in lack of appetite, with age, marital status, BMI, marijuana use, and total symptom burden remaining significant independent correlates (p’ s <.01). Conclusions: Contrary to expectations, relatively few clinical correlates were associated with self-reported lack of appetite. Future research should explore inter-individual genetic factors to explain alterations in lean body mass and body weight that may contribute to poor appetite in patients. Such factors may be important indicators for early identification of CACS.

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