Parathyroid Hormone and Calcitonin: Influences upon Lipolysis of Human Adipose Tissue

Gozariu, L; K, Forster; Jd, Faulhaber; Minne, H; Ziegler, Rudolf

doi:10.1055/s-0028-1095713

Cited by 19 publications

(5 citation statements)

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“…This ,8-blocking agent had no effect on the 1- (5)(6)(7)(8)(9)(10). It has been shown that parathyroid hormone can promote lipolysis in human adipocytes (14,15 (14,15). These hormone concentrations are unplhysiologically high.…”

Section: Introductionmentioning

confidence: 91%

Adenylate cyclase of human fat cell ghosts. Stimulation of enzyme activity by parathyroid hormone.

Kather¹,

Simon²

1977

J. Clin. Invest.

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A B S T R A C T Some of the effects of native bovineparathyroid hormone and of the synthetic aminoterminal 1-34 fragment on the adenylate cyclase activity of human fat cell ghosts were studied. Saturating concentrations of both hormone preparations caused a significant increase of enzyme activity by about 200-300%. Guanosine 5'-triphosphate (0.1 mM) inhibited basal enzyme activity but had no substantial effect on parathyroid hormone-stimulated enzyme activity. The guanosine 5'-triphosphate analogue, 5'-guanylyl-imidodiphosphate, produced about a threefold enhancement of basal and parathyroid hormone-stimulated enzyme activities under standard conditions (5 mM Mg2+, 1 mM ATP, pH 8.0, 30°C).Activation by parathyroid hormone was not influenced by 83-adrenergic blockade in contrast to stimulation by epinephrine. The sensitivity of the enzyme system to the native and the synthetic parathyroid hormone was, however, abolished after pretreatment of the fat cells with trypsin (1 mg/ml). The stimulatory effects of epinephrine and NaF were not affected by pretreatment with trypsin.The results suggest that human fat cells, like rat adipocytes, contain a multireceptor-coupled adenylate cyclase.

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Section: Introductionmentioning

confidence: 91%

Adenylate cyclase of human fat cell ghosts. Stimulation of enzyme activity by parathyroid hormone.

Kather¹,

Simon²

1977

J. Clin. Invest.

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“…PTH promotes mobilization of calcium from bone by increasing bone resorption and the kidney's production of 1,25-dihydroxyvitamin D in conditions of serum hypocalcemia (de Paula and Rosen 2010). Both singledose and intermittent PTH treatments stimulate lipolysis of white adipose tissue and the production of glycerol in a dose-dependent manner, also linking PTH and adiposity (Gozariu et al 1974;Sinha et al 1976). Intermittent PTH treatment inhibits the differentiation of adipocytes (Rickard et al 2006;Kulkarni et al 2007).…”

Section: Parathyroid Hormonementioning

confidence: 99%

Endocrine Regulation of Bone and Energy Metabolism in Hibernating Mammals

Doherty

Florant

Donahue

2014

Integrative and Comparative Biology

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Precise coordination among organs is required to maintain homeostasis throughout hibernation. This is particularly true in balancing bone remodeling processes (bone formation and resorption) in hibernators experiencing nutritional deprivation and extreme physical inactivity, two factors normally leading to pronounced bone loss in non-hibernating mammals. In recent years, important relationships between bone, fat, reproductive, and brain tissues have come to light. These systems share interconnected regulatory mechanisms of energy metabolism that potentially protect the skeleton during hibernation. This review focuses on the endocrine and neuroendocrine regulation of bone/fat/energy metabolism in hibernators. Hibernators appear to have unique mechanisms that protect musculoskeletal tissues while catabolizing their abundant stores of fat. Furthermore, the bone remodeling processes that normally cause disuse-induced bone loss in non-hibernators are compared to bone remodeling processes in hibernators, and possible adaptations of the bone signaling pathways that protect the skeleton during hibernation are discussed. Understanding the biological mechanisms that allow hibernators to survive the prolonged disuse and fasting associated with extreme environmental challenges will provide critical information regarding the limit of convergence in mammalian systems and of skeletal plasticity, and may contribute valuable insight into the etiology and treatment of human diseases.

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“…It has been shown that parathyroid hormone (PTH) can promote lipolysis in h u m a n lipocytes [2,11]. We were recently able to demonstrate that the adenylate cyclase system of human fat cell ghosts reacts to at least t w o different classes of hormones:…”

Section: Lipolysismentioning

confidence: 99%

Human fat cell adenylate cyclase

1977

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The effects of guanine nucleotides on basal and parathyroid hormone-stimulated adenylate cyclase of human fat cell ghosts were studied. GTP (10(-7)-10(-3) M) caused a dose-dependent inhibition of basal enzyme activity, but it had no significant effect on PTH-stimulated rates of cAMP-formation. The guanine nucleotide analogue 5'-guanylyl-imidodiphosphate GMP (PNP) when applied in the same concentration range, stimulated basal as well as PTH-activated adenylate cyclase activity up to 300%. GMP (PNP) activation was non-linear with time. PTH-activated the human fat cell adenylate cyclase via an individual receptor distinct from beta-adrenergic receptor sites.

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Parathyroid Hormone and Calcitonin: Influences upon Lipolysis of Human Adipose Tissue

Cited by 19 publications

References 0 publications

Adenylate cyclase of human fat cell ghosts. Stimulation of enzyme activity by parathyroid hormone.

Adenylate cyclase of human fat cell ghosts. Stimulation of enzyme activity by parathyroid hormone.

Endocrine Regulation of Bone and Energy Metabolism in Hibernating Mammals

Human fat cell adenylate cyclase

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