Orderliness of hormone release patterns: a complementary measure to conventional pulsatile and circadian analyses

Veldhuis, Johannes D.; Pincus, Steven M.

doi:10.1530/eje.0.1380358

Cited by 84 publications

(42 citation statements)

References 26 publications

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“…This function quantifies non-pulsatile and non-circadian regulation of hormone secretion (46). Leptin ApEn values were similar in patients and controls, which signifies comparable feedback and feedforward control of leptin secretion.…”

Section: Discussionmentioning

confidence: 74%

Hyperleptinemia in women with Cushing's disease is driven by high-amplitude pulsatile, but orderly and eurhythmic, leptin secretion

Veldman¹,

Frölich

Pincus

et al. 2001

European Journal of Endocrinology

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The episodicity of 24 h leptin release was studied in seven women (mean age 39 years, range 22±56 years) with pituitary-dependent hypercortisolism and in seven age-and body mass index (BMI)-matched female controls. Pulsatile leptin release was quantified by model-free CLUSTER analysis and deconvolution, the orderliness of leptin patterns by the approximate entropy statistic (ApEn), and nyctohemeral leptin rhythmicity by cosinor analysis. Blood samples were taken at 10 min intervals for 24 h. Both CLUSTER and deconvolution analysis revealed 2.4-fold increased leptin secretion in patients, caused by combined and equal amplification of basal and pulsatile secretion. Cluster analysis identified 7X1^1X5 peaks per 24 h in patients and 6X0^0X5 in controls (not significant). The statistical distribution of the individual sample secretory rates was similarly skewed in patients and controls 0X55^0X12 vs 0X52^0X07X The acrophase (timing of the nyctohemeral leptin peak) in patients occurred at 2314 h (^76 min) and at 0058 h (^18 min) in controls (not significant). The approximate entropy of leptin release was equivalent in patients and controls 1X67^0X03 vs 1X610 X05X The approximate entropy (ApEn) for cortisol in patients was 1X53^0X09 and in controls was 0X93^0X07 P , 0X0005X Cross-ApEn showed significant pattern synchrony between leptin and cortisol release, which (unexpectedly) was not disrupted by the cortisol excess (patients, 2X02^0X04; controls, 1X88^0X09; P 0X233X Insulin levels in fasting patients (`fasting insulin') were 275 X7 mUal vs 14^1X6 mUal in controls P 0X035X Leptin secretion correlated with fasting insulin levels R 2 0X34Y P 0X028 and with the cortisol production rate R 2 0X33Y P 0X033 when patients and controls were combined. In summary, Cushing's disease in women increases leptin production about twofold in an amplitude-specific way. The pulse-generating, nyctohemeral phasedetermining, and entropy-control mechanisms that govern the 24 h leptin release are not altered. The increased secretion is not explained by BMI and is probably only partly explained by increased insulin production, suggesting a cortisol-dependent change in adipose leptin secretion.

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Section: Discussionmentioning

confidence: 74%

Hyperleptinemia in women with Cushing's disease is driven by high-amplitude pulsatile, but orderly and eurhythmic, leptin secretion

Veldman¹,

Frölich

Pincus

et al. 2001

European Journal of Endocrinology

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“…ApEn and cross-ApEn data were presented as a normalized ratio defined by the mean ratio of absolute value to that of 1,000 randomly shuffled versions of the same time sequences (43).…”

Section: Diurnal Variability Analysismentioning

confidence: 99%

Alterations in the dynamics of circulating ghrelin, adiponectin, and leptin in human obesity

Yildiz

Suchard

Wong

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

322

219

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Ghrelin plays a key role in the regulation of growth hormone secretion and energy homeostasis. Adiponectin is exclusively secreted by adipose tissue and is abundantly present in the circulation, with important effects on metabolism. We studied five lean and five obese young men [ages: 24.2 ؎ 1.0 (lean) and 21.8 ؎ 1.6 (obese) years (difference not significant); body mass indexes: 35.0 ؎ 1.3 and 23.0 ؎ 0.3 kg͞m 2 (P ‫؍‬ 0.01)], sampled blood every 7 min over 24 h, and measured ghrelin, adiponectin, and leptin in 2,070 samples for a total of 6,210 data points. Circulating 24-h ghrelin showed significant ultradian fluctuations and an orderly pattern of release in lean and obese subjects with similar pulsatility characteristics. Plasma adiponectin concentrations were significantly lower in the obese group, with lower pulse height. In contrast to leptin, which is secreted in an orderly manner, the 24-h patterns of adiponectin were not significantly different from random in both the lean and obese groups. We show here that adipocytes can simultaneously secrete certain hormones, such as leptin, in patterns that are orderly, whereas other hormones, such as adiponectin, are secreted in patterns that appear to be random. The cross-approximate entropy statistic revealed pattern synchrony among ghrelin-leptin, ghrelin-adiponectin, and leptinadiponectin hormone time series in the lean and obese subjects. Plasma ghrelin concentrations showed a nocturnal rise that exceeded the meal-associated increases in lean subjects, and this newly identified nocturnal rise was blunted in the obese. We suggest that the blunting of the nocturnal rise of ghrelin is a biological feature of human obesity.

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“…Hence, this member of the ApEn family is designated ApEn (1, 20%). The ApEn metric evaluates the consistency of recurrent subordinate (nonpulsatile) patterns in a time series and therefore yields information distinct from and complementary to cosinor and deconvolution (pulse) analyses (13). Higher absolute ApEn values denote greater relative randomness of hormone patterns.…”

Section: Twenty-four Hour Plasma Hormone Profilesmentioning

confidence: 99%

Growth hormone secretion and immunological function of a male patient with a homozygous STAT5b mutation

et al. 2007

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Objective: STAT5b is a component of the GH signaling pathway. Recently, we described a 31-year-old male patient (height, K5.9 SDS) with a novel homozygous inactivating mutation in the STAT5b gene. The purpose of this study is to describe the phenotype in detail, including GH secretion and immunological function. In addition, we report four family members of this patient, all heterozygous carriers of the mutation. Design and methods: Twenty-four hour GH and prolactin secretion characteristics were assessed by blood sampling at 10-min intervals. An IGF-I generation test was performed. Monocyte function was tested by stimulation of whole blood with lipopolysaccharide (LPS) in the presence or absence of Interferon-g (IFN-g). In addition, T cell function was determined by measuring proliferative responses of peripheral blood mononuclear cells (PBMC) after stimulation by various polyclonal activators and Interleukin-2 (IL-2). Clinical and biochemical characteristics were determined in the carriers of the mutation. Results: GH secretory parameters were comparable with that of healthy male controls (mean fat percentage 25), but likely increased in relation to the patient's 40% body fat. The regularity of GH secretion was diminished. Prolactin secretion was increased by sixfold. The IGF-I generation test showed a small increase in IGF-I and IGF-binding protein-3 on lower GH doses and an increase in IGF-I to K2.4 SDS on the highest dose of GH. In vitro, IL-12p40, IL 10, and tumour necrosis factor-a (TNF-a) production rates by PBMC increased to values within the normal range upon stimulation of LPS. Heterozygous carriers of the mutation did not show abnormalities, although the height of the males was below the normal range. Conclusions: This report shows that GH and prolactin secretion were increased in this patient homozygous for a new STAT5b mutation. Although STAT5b plays a role in signaling within immune cells, clinical immunodeficiency is not an obligatory phenomenon of STAT5b deficiency per se. Heterozygous carriers of a STAT5b mutation show no signs of GH insensitivity. 156 155-165 European Journal of Endocrinology

show abstract

Orderliness of hormone release patterns: a complementary measure to conventional pulsatile and circadian analyses

Cited by 84 publications

References 26 publications

Hyperleptinemia in women with Cushing's disease is driven by high-amplitude pulsatile, but orderly and eurhythmic, leptin secretion

Hyperleptinemia in women with Cushing's disease is driven by high-amplitude pulsatile, but orderly and eurhythmic, leptin secretion

Alterations in the dynamics of circulating ghrelin, adiponectin, and leptin in human obesity

Growth hormone secretion and immunological function of a male patient with a homozygous STAT5b mutation

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