Growth Hormone (GH) Replacement Reduces Total Body Fat and Normalizes Insulin Sensitivity in GH-Deficient Adults: A Report of One-Year Clinical Experience

1997 ◽  
Vol 82 (10) ◽  
pp. 3285-3292 ◽  
Author(s):  
C.-M. Hwu
1997 ◽  
Vol 82 (10) ◽  
pp. 3285-3292
Author(s):  
Chii-Min Hwu ◽  
Ching Fai Kwok ◽  
Tzong-Yoe Lai ◽  
Kuang-Chung Shih ◽  
Tian-Shing Lee ◽  
...  

2002 ◽  
Vol 103 (4) ◽  
pp. 391-396 ◽  
Author(s):  
Fiona E. ARROWSMITH ◽  
Julie WARD ◽  
Kieron ROONEY ◽  
Adamandia D. KRIKETOS ◽  
Louise A. BAUR ◽  
...  

Muscle blood flow can be reduced in insulin-resistant states. The present study examined the importance of body fatness and insulin sensitivity as variables that may be associated with muscle oxygen supply. We studied 38 adolescents (22 males, 16 females; age 15.3–18.6 years; body mass index 17.7–34.7kg/m2) and used near-IR spectroscopy to measure the muscle re-oxygenation rate after ischaemic finger flexion exercise. Total body fat content was estimated by bioelectrical impedance analysis, and insulin sensitivity was assessed by homoeostasis model assessment. Regional lipid compartments were also assessed for potential associations with muscle oxygen supply. Abdominal adiposity (visceral and subcutaneous) was assessed by magnetic resonance imaging, and soleus intramyocellular lipid levels were determined by magnetic resonance spectroscopy. Total body fat content (r = 0.67, P<0.001), abdominal subcutaneous fat area (r = 0.78, P<0.001), abdominal visceral fat area (r = 0.54, P<0.001) and intramyocellular lipid levels (r = 0.68, P<0.001) were significantly related to forearm re-oxygenation half-time. After adjusting for insulin sensitivity, both total body fat content (r = 0.395, P = 0.02) and abdominal subcutaneous fat area (r = 0.543, P = 0.001) remained positively associated with relatively reduced muscle oxygen supply in adolescent subjects. After adjusting for body fat content, abdominal subcutaneous fat area (r = 0. 511, P = 0.002) was significantly associated with muscle oxygen supply. Thus muscle oxygen supply is associated with body fat content, and certain fat compartments may be more influential than others.


2018 ◽  
Vol 50 (09) ◽  
pp. 675-682 ◽  
Author(s):  
Patrícia Tosta-Hernandez ◽  
Adriana Siviero-Miachon ◽  
Nasjla da Silva ◽  
Andrea Cappellano ◽  
Marcelo Pinheiro ◽  
...  

AbstractCraniopharyngioma is a sellar/suprasellar benign tumor whose aggressiveness may imply in endocrine disturbances (hypothalamic obesity and hormone deficiencies). Fifty-seven patients were evaluated according to clinical characteristics, hypothalamic involvement, type of treatment, anthropometric variables, adiposity indexes (body mass index Z score category at diagnosis and post-treatment, total body fat, visceral adipose tissue, and metabolic syndrome components) and analyzed through multiple regression and logistic models. Patients were stratified according to growth hormone deficiency and recombinant human growth hormone use. Mean ages at diagnosis and at study evaluation were 9.6 and 16.6 years old, respectively. A set of 43/57 (75.4%) patients presented with important hypothalamic involvement, 24/57 (42.1%) received surgical treatment and cranial radiotherapy, and 8/57 (14%) interferon-α exclusively. Fifty-five patients (96.5%) were considered growth hormone deficient, and 26/57 (45.6%) grew despite no recombinant human growth hormone replacement therapy. At diagnosis, 12/57 (21%) patients were obese, and 33/57 (57.9%) at study evaluation, and after 3.2 years (median) post first therapy. There was no influence of height Z score on body mass index Z score. Body mass index Z score at diagnosis positively influenced body mass index Z score, total body fat, waist circumference and the presence of the metabolic syndrome post-treatment. Replacement of recombinant human growth hormone decreased total body fat and visceral adipose tissue. Craniopharyngioma patients worsened body mass index Z score category 3.2 years (median) after first treatment. Body mass index Z score increased due to real weight gain, without height decrease. Replacement of recombinant human growth hormone had beneficial effect on adiposity.


2009 ◽  
Vol 102 (2) ◽  
pp. 195-200 ◽  
Author(s):  
Anne-Sophie Morisset ◽  
Simone Lemieux ◽  
Alain Veilleux ◽  
Jean Bergeron ◽  
S. John Weisnagel ◽  
...  

There has been a growing interest in lignans, a class of phyto-oestrogens, because of their potentially favourable effects on human health. The aim of the present study was to compare the metabolic profile of post-menopausal women consuming various amounts of dietary lignans. Phyto-oestrogen intake was assessed using a 3-d dietary record analysed with a Canadian food phyto-oestrogen content data table in 115 post-menopausal women (age 56·8 (sd 4·4) years and BMI 28·5 (sd 5·9) kg/m2). Plasma enterolactone (ENL), the major biologically active metabolite of dietary lignans, was determined by time-resolved fluoroimmunoassay. Anthropometrics, abdominal adipose tissue areas (computed tomography), body composition (hydrostatic weighing) and insulin sensitivity (hyperinsulinaemic–euglycaemic clamp) were measured in all women. Women in the high dietary lignan intake subgroup (n 29) had a significantly lower BMI and total body fat mass, as well as a better glucose disposal rate (GDR; P < 0·05), compared with women in the low lignan intake subgroup (n 28). The majority of women with the highest dietary lignan intake were also in the highest quartile of plasma ENL (59 %). Women in the highest ENL quartile had a significantly lower BMI (26·1 (sd 4·4) v. 30·4 (sd 6·9) kg/m2, P < 0·05), total body fat mass (24·8 (sd 9·8) v. 33·3 (sd 13·3) kg, P < 0·05), 2 h postload glycaemia (5·5 (sd 0·9) v. 5·7 (sd 0·8) nmol/l, P < 0·05) and a higher GDR (8·3 (sd 2·7) v. 5·5 (sd 2·8), P < 0·01) compared with women in the lowest ENL quartile. In conclusion, women with the highest ENL concentrations had a better metabolic profile including higher insulin sensitivity and lower adiposity measures.


2013 ◽  
Vol 28 (5) ◽  
pp. 1489-1493 ◽  
Author(s):  
Alessandro Mor ◽  
Lawrence Tabone ◽  
Philip Omotosho ◽  
Alfonso Torquati

2001 ◽  
pp. 711-716 ◽  
Author(s):  
JA Janssen ◽  
FM van der Toorn ◽  
LJ Hofland ◽  
P van Koetsveld ◽  
F Broglio ◽  
...  

OBJECTIVE: Ghrelin stimulates growth hormone (GH) secretion both in vivo and in vitro. Ghrelin is mainly produced in and released from the stomach but it is probably also produced in the hypothalamic arcuate nucleus. Whether pituitary GH release is under the control of ghrelin from the stomach and/or from the arcuate nucleus is not known. Moreover, no data on the feedback of GH on systemic ghrelin concentrations are available. It has recently been suggested that ghrelin may induce obesity. DESIGN: In this study, we addressed the following two questions: a) are circulating ghrelin levels increased in human GH deficiency (GHD), and b) does GH treatment modify ghrelin levels in human GHD? METHODS: The study group consisted of 23 patients with GHD. Eighteen had developed adult-onset GHD and five had developed GHD in their childhood (childhood-onset GHD). Ghrelin was measured with a commercially available radioimmunoassay. All measurements were performed twice, first at baseline, before the start of GH replacement therapy, and then again after one year of therapy. GH doses were adjusted every 3 months, targeting serum total IGF-I levels within the normal gender- and age-related reference values for the healthy population. Maintenance doses were continued once the target serum total IGF-I levels were reached. RESULTS: The sum of skinfolds and body water increased significantly, body fat mass and percentage body fat decreased significantly and body mass index and waist-hip ratio were not significantly changed by one year of GH replacement therapy.Before the start of GH replacement therapy, mean value and range for fasting ghrelin in the studied GHD subjects tended to be lower in comparison with healthy subjects in the control group although the difference did not reach significance (GHD ghrelin mean 67.8 pmol/l, range 37.6-116.3 pmol/l; control mean 83.8 pmol/l, range 35.4-132 pmol/l; P=0.11).One year of GH replacement therapy did not modify circulating ghrelin levels (ghrelin before GH therapy: 67.8 pmol/l, range 37.6-116.3 pmol/l; after GH therapy: 65.3 pmol/l, range 35.8-112.6; P=0.56). CONCLUSIONS: We did not observe elevated ghrelin levels in adult GHD subjects and GH replacement therapy did not modify circulating ghrelin levels, despite significant decreases in body fat mass and percentage body fat. It is conceivable that the lack of ghrelin modifications after long-term GH therapy was due to the reduction of adiposity and insulin on one hand, and increased GH secretion on the other. However, it is still possible that systemic ghrelin is involved in the development of obesity, both in normal and GHD subjects.


2004 ◽  
Vol 89 (3) ◽  
pp. 1391-1396 ◽  
Author(s):  
Johan Hoffstedt ◽  
Elisabet Arvidsson ◽  
Eva Sjölin ◽  
Kerstin Wåhlén ◽  
Peter Arner

Abstract The role of adiponectin production for the circulating protein concentration in human obesity and insulin resistance is unclear. We measured serum concentration and sc adipose tissue secretion rate of adiponectin in 77 obese and 23 nonobese women with a varying degree of insulin sensitivity. The serum adiponectin concentration was similar in both groups. In obesity, adiponectin adipose tissue secretion rate per weight unit was reduced by 30% (P = 0.01), whereas total body fat secretion rate was increased by 100% (P &lt; 0.0001). In the group being most insulin resistant (1/3), serum concentration (P &lt; 0.001) and adipose tissue secretion rate per tissue weight (P &lt; 0.05) were reduced, whereas total body fat secretion rate was increased (P &lt; 0.01), by about 30%. The adipose tissue secretion rate of adiponectin was related to the serum concentration (P = 0.005) but explained only about 10% of the interindividual variation in circulating adiponectin and insulin sensitivity. The plasma adiponectin half life was long, 2.5 h. In conclusion, the role of protein secretion for the circulating concentration of adiponectin and insulin sensitivity under these conditions is minor because adiponectin turnover rate is slow. Although increased in obesity and insulin resistance, total body production of adiponectin is insufficient to raise the circulating concentration, may be due to reduced secretion rate per tissue unit.


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