Demonstration that Cyclic Adenosine 3',5'-Monophosphate Mediates the Lipolytic Action of Parathyroid Hormone

Abstract

Studies were carried out with rat epididymal fat pads first to compare the effects of the synthetic N-terminal 1-34 peptide of bovine parathyroid hormone and of the native hormone to determine whether this portion of the molecule is responsible for the lipolytic action of the hormone and second to determine whether this biologic action of parathyroid hormone is mediated by cyclic adenosine 3',5'-monophosphate. The N-terminal polypeptide was as effective as the native hormone in stimulating lipolysis in the concentration range between 10(-8) M and 10(-6) M. Parathyroid hormone stimulated lipolysis by isolated fat cells. The concentration of cyclic adenosine 3',5'-monophosphate in the fat pads was significantly increased by the hormone (10(-6)M). Lipolytic stimulation by parathyroid hormone (10(-6)M) was diminished by insulin (100 muU/ml) and prostaglandin E1 (1 mug/ml), both of which are known inhibitors of lipolysis. The findings indicate that the amino-terminal 1-34 peptide portion of parathyroid hormone is responsible for the lipolytic action and that this effect is mediated through cyclic adenosine 3',5'-monophosphate.

Parathyroid hormone induces a browning program in human white adipocytes

“…Although very little is known about PTH signaling in adipose tissue, already more than 40 years ago it was reported that PTH induces lipolysis in rat and human fat explants with increased production of cAMP 20, 21. More recently, it was discovered that PTH promotes adipocyte lipolysis through cAMP-dependent activation of the PKA pathway, a downstream signal of the PTH receptor 13.…”

Adipose tissue energy metabolism: altered gene expression profile of mice subjected to long‐term caloric restriction

“…LCR altered the expression of five genes encoding lipolysis-related proteins ( Table 4). β3-Adrenergic signals (1,2,42), parathyroid hormone (43), and growth hormone (44) promote lipolytic activities through their receptors. The receptors, β3-adrenergic receptor (b3ADr) and parathyroid hormone receptor (PTHr), were up-regulated by LCR, whereas low molecular weight growth hormone receptor/binding protein was down-regulated.…”