No abstract available.
Leptin* ; Metabolism*

No abstract available.
Eating* ; Glucose* ; Leptin* ; Metabolism* ; Resistin*

Leptin, a 167-amino acid peptidic hormone encoded by the obese gene, is known to be involved in the regulation of body fat, energy expenditure, immune function, angiogenesis, inflammatory reaction, the onset of puberty, and the regulation of reproductive function. The roles of leptin vary with different expression and distribution patterns of its receptor Ob-R. This article analyzes the biological effects of leptin and its receptor on the testis by reviewing the expression and distribution of Ob-R in different cells during different developmental stages or in different physiological and pathological states in the testis of men, mice or rats.
Animals ; Humans ; Male ; Mice ; Rats ; Receptors, Leptin ; metabolism ; Testis ; metabolism

Leptin, an adipocyte-derived peptide hormone, has been shown to facilitate breathing. However, the central sites and circuit mechanisms underlying the respiratory effects of leptin remain incompletely understood. The present study aimed to address whether neurons expressing leptin receptor b (LepRb) in the nucleus tractus solitarii (NTS) contribute to respiratory control. Both chemogenetic and optogenetic stimulation of LepRb-expressing NTS (NTS^LepRb) neurons notably activated breathing. Moreover, stimulation of NTS^LepRb neurons projecting to the lateral parabrachial nucleus (LPBN) not only remarkably increased basal ventilation to a level similar to that of the stimulation of all NTS^LepRb neurons, but also activated LPBN neurons projecting to the preBötzinger complex (preBötC). By contrast, ablation of NTS^LepRb neurons projecting to the LPBN notably eliminated the enhanced respiratory effect induced by NTS^LepRb neuron stimulation. In brainstem slices, bath application of leptin rapidly depolarized the membrane potential, increased the spontaneous firing rate, and accelerated the Ca²⁺ transients in most NTS^LepRb neurons. Therefore, leptin potentiates breathing in the NTS most likely via an NTS-LPBN-preBötC circuit.
Leptin/pharmacology* ; Membrane Potentials ; Neurons/metabolism* ; Solitary Nucleus/metabolism*

OBJECTIVETo investigate the expressions of leptin and its receptor in the epididymis of experimental varicocele (EV) rats.

METHODSForty male Sprague-Dawley rats were randomly divided into four groups: 4-week EV (n = 12), 8-week EV (n = 12), 4-week control (n = 8), and 8-week control (n = 8). EV models were established by partial ligation of the left renal vein. The expressions of leptin and its receptor in the rat epididymis were measured by immunohistochemistry, and their mRNA expressions determined by real-time quantitative PCR.

RESULTSThe expressions of leptin and its receptor in the epididymis were significantly higher in the 4- and 8-week EV groups than in the 4- and 8-week control groups (P < 0.01), with no significant difference between the two EV groups (P > 0.05). So were their mRNA expressions in the former two than in the latter two groups (P < 0.01), with no significant difference between the former two (P > 0.05).

CONCLUSIONThe expressions of leptin and its receptor are markedly increased in the epididymis of varicocele rats. Leptin may be involved in the mechanisms of varicocele inducing male infertility.

Animals ; Disease Models, Animal ; Epididymis ; metabolism ; Leptin ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Receptors, Leptin ; metabolism ; Varicocele ; metabolism

OBJECTIVETo investigate the expressions of leptin and leptin receptor in hepatocellular carcinoma (HCC) and explore the clinicopathological significance.

METHODSThe expressions of leptin and leptin receptor were examined by immunohistochemistry in 81 HCC patients undergoing curative tumor resection. The correlations between the expression of two biomarkers and the clinicopathological factors were analyzed.

RESULTSThe overexpression rate of leptin and leptin receptor in HCC was 56.8% and 35.8%, respectively. No significant correlation was observed between their overexpression (r=0.236, P=0.034). Leptin receptor overexpression was significantly correlated to the tumor size and TNM stage (P<0.05), but not to age, body mass index, α-fetoprotein, hepatitis B surface antigen status, tumor grade, vascular invasion, or liver cirrhosis (P≥0.05). Leptin overexpression showed no significant correlations to the above clinicopathological factors (P≥0.05).

CONCLUSIONLeptin receptor overexpression may have an inhibitory effect on hepatocellular carcinoma. The expression status of leptin receptor decides the action of leptin and leptin receptor after their binding.

Carcinoma, Hepatocellular ; metabolism ; pathology ; Female ; Humans ; Leptin ; metabolism ; Liver Neoplasms ; metabolism ; pathology ; Male ; Middle Aged ; Neoplasm Staging ; Receptors, Leptin ; metabolism

The prevailing model of osteology is that bones constantly undergo a remodeling process, and that the differentiation and functions of osteoblasts are partially regulated by leptin through different central hypothalamic pathways. The finding that bone remodeling is regulated by leptin suggested possible endocrinal effects of bones on energy metabolism. Recently, a reciprocal relationship between bones and energy metabolism was determined whereby leptin influences osteoblast functions and, in turn, the osteoblast-derived protein osteocalcin influences energy metabolism. The metabolic effects of bones are caused by the release of osteocalcin into the circulation in an uncarboxylated form due to incomplete gamma-carboxylation. In this regard, the Esp gene encoding osteotesticular protein tyrosine phosphatase is particularly interesting because it may regulate gamma-carboxylation of osteocalcin. Novel metabolic roles of osteocalcin have been identified, including increased insulin secretion and sensitivity, increased energy expenditure, fat mass reduction, and mitochondrial proliferation and functional enhancement. To date, only a positive correlation between osteocalcin and energy metabolism in humans has been detected, leaving causal effects unresolved. Further research topics include: identification of the osteocalcin receptor; the nature of osteocalcin regulation in other pathways regulating metabolism; crosstalk between nutrition, osteocalcin, and energy metabolism; and potential applications in the treatment of metabolic diseases.
Bone Remodeling/physiology ; Bone and Bones/*metabolism ; *Energy Metabolism ; Humans ; Leptin/metabolism ; Osteocalcin/genetics/*metabolism

To study the expression and distribution of neuropeptide Y (NPY) and long leptin receptor (OB-Rb) in the gastrointestinal tract of giant panda, samples of three animals were collected from the key laboratory for reproduction and conservation genetics of endangered wildlife of Sichuan province, China conservation and research center for the giant panda. Paraffin sections of giant panda gastrointestinal tissue samples were observed using hematoxylin-eosin staining (HE) and strept actividin-biotin complex immunohistochemical staining (IHC). The results show that the intestinal histology of three pandas was normal and no pathological changes, and there were rich single-cell and multi-cell mucous glands, long intestinal villi and thick muscularis mucosa and muscle layer. Positive cells expressing NPY and OB-Rb were widely detected in the gastrointestinal tract by IHC methods. NPY positive nerve fibers and neuronal cell were widely distributed in submucosal plexus and myenteric plexus, especially in the former. They were arranged beaded or point-like shape. NPY positive cells were observed in the shape of ellipse and polygon and mainly located in the mucous layer and intestinal glands. OB-Rb positive cells were mainly distributed in the mucous layer and the laminae propria, especially the latter. These results confirmed that NPY and OB-Rb are widely distributed in the gut of the giant panda, which provide strong reference for the research between growth and development, digestion and absorption, and immune function.
Animals ; China ; Intestines ; metabolism ; Neuropeptide Y ; genetics ; metabolism ; Receptors, Leptin ; genetics ; metabolism ; Ursidae ; genetics ; metabolism

Adult ; Endometriosis ; complications ; metabolism ; Endometrium ; metabolism ; Female ; Humans ; Infertility, Female ; etiology ; metabolism ; Leptin ; metabolism

PURPOSE: The adipocyte-derived cytokine leptin plays a major role in the control of stable body weight by suppressing food intake and increasing energy metabolism. Leptin regulates the cell proliferation of various epithelial cells and it may be involved in the promotion of cancer. Leptin and its receptor are highly expressed in gastric adenocarcinoma, but the association between the serum leptin level and the tissue expression of leptin is uncertain. We evaluated the serum leptin level and the expressions of leptin and leptin receptor in gastric cancer, and we explore the possible mechanism and role of leptin in the carcinogenesis of gastric cancer. MATERIALS AND METHODS: 72 carcinomas that were curatively resected at our hospital from October 2005 to March 2007 were included in this study. By immunoassay and immunohistochemical staining, we evaluated the serum leptin level and the expressions of leptin and its receptor, and we analyzed their relationship together with the clinicopathological variables. RESULTS: The serum leptin level was increased as the patient's BMI increased and it was decreased in H. pylori infected patients. The expression of leptin was increased as the TNM stage increased (P=0.014), and the expression of leptin receptor in the intestinal type gastric adenocarcinoma was higher than that in the diffuse type gastric adenocarcinoma (71.4% vs 28.6%, respectively, P=0.033). CONCLUSION: There was no significant correlation between the serum leptin level and expression of leptin in gastric cancer patients. The expression of leptin was associated with the TNM stage, but its role in the pathogenesis of gastric cancer has to be elucidated.
Adenocarcinoma ; Body Weight ; Cell Proliferation ; Eating ; Energy Metabolism ; Epithelial Cells ; Humans ; Immunoassay ; Leptin ; Receptors, Leptin ; Stomach ; Stomach Neoplasms