leptin and Gastroparesis

Anorexia during infection is thought to be mediated by immunoregulatory cytokines such as interleukins 1 and 6 and tumor necrosis factor. This article reviews the potential mechanisms of action by which these cytokines are thought to suppress food intake during infection and examines the proposition that blocking of cytokine activity might be one approach to improving food intake of the infected host.

Topics: Acute-Phase Reaction; Animals; Anorexia; Cholecystokinin; Cytokines; Dinoprostone; Disease Models, Animal; Eating; Fever; Gastroparesis; Humans; Infections; Inflammation Mediators; Leptin; Vagus Nerve

Gastrointestinal complications in diabetes may affect glucose and endocrine homeostasis. Glucose-dependent insulinotropic peptide (GIP), glucagon-like peptide-1 (GLP-1), and leptin regulate glucose homeostasis, food intake, and gastric emptying.. The aim was to investigate associations between diabetes complications and glucose homeostasis and plasma levels of GIP, GLP-1, and leptin.. Sixteen diabetes patients (seven men) were examined with gastric emptying scintigraphy and 72-h continuous subcutaneous glucose monitoring, 14 with the deep-breathing test, and 12 with esophageal manometry. A fiber-rich breakfast was given during the second day of glucose registration. Blood samples were taken 10 min and right before a fat-rich breakfast, as well as 10, 20, 30, 45, 60, 90, 120, 150, and 180 min afterwards. 20 healthy volunteers acted as controls. Plasma was analyzed regarding GIP, GLP-1, and leptin by Luminex.. Gastroparesis lowered maximal concentration (c-max) (p = 0.003) and total area under the curve (tAUC) (p = 0.019) of glucose levels as well as d-min (p = 0.043) of leptin levels. It tended to lower baseline (p = 0.073), c-max (p = 0.066), change from baseline (d-max) (p = 0.073), and tAUC (p = 0.093) of GLP-1 concentrations. Esophageal dysmotility tended to lower tAUC of glucose levels (p = 0.063), and c-min (p = 0.065) and tAUC (p = 0.063) of leptin levels. Diabetes patients had a higher baseline concentration of glucose (p = 0.013), GIP (p = 0.023), and leptin (p = 0.019) compared with healthy subjects.. Gastric and esophageal dysmotility are associated with both lesser increases in postprandial glucose elevations and decreased postprandial changes in GLP-1 and leptin.

Topics: Adult; Blood Glucose; Diabetes Mellitus, Type 2; Esophageal Motility Disorders; Female; Gastric Inhibitory Polypeptide; Gastroparesis; Glucagon-Like Peptide 1; Humans; Insulin; Leptin; Male; Middle Aged; Postprandial Period

Diabetic gastroparesis (DG) is a common clinical complication of diabetes mellitus. Leptin may cause delayed gastric emptying in the central and peripheral pathways. Microcirculatory disturbances in the stomach make gastric smooth muscles and nerves hypoxic-ischemic, thereby impairing gastric motility. Irbesartan is an angiotensin II (ATII) receptor blocker that indirectly decreases serum leptin levels and improves blood vessel endothelia. This study examined the effect of irbesartan on DG and its relationship with serum leptin levels and microcirculatory disturbances of the stomach. Sprague-Dawley rats were injected with streptozotocin to induce diabetes and were then treated with or without 0.012 g·kg(-1)·d(-1) irbesartan by gavage. After six weeks of treatment, the gastric evacuation rate (GER) was measured using phenol red. Serum leptin levels were detected using enzyme-linked immunosorbent assays. Endothelin (ET) in the stomach tissue was examined using a radioimmunoassay, whereas chemical colorimetry was used to measure the nitric oxide synthase (NOS) activity of stomach tissues. The mRNA expression of the ATII receptor (AT1R) was assessed using reverse transcription-polymerase chain reaction. Treatment with irbesartan significantly increased the GER of diabetic rats and reduced the serum leptin levels, as well as decreased the ET content and AT1R mRNA expression in the stomach (P<0.05). Changes in the cNOS activity after irbesartan intervention were not significant (P>0.05), whereas iNOS activity was significantly decreased (P<0.05). Irbesartan can alleviate hyperglycemia-induced delayed gastric emptying, which is associated with decreased serum leptin levels and improved microcirculation in the stomach.

Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Biphenyl Compounds; Blood Glucose; Diabetes Complications; Diabetes Mellitus, Experimental; Disease Models, Animal; Gastric Emptying; Gastroparesis; Gene Expression; Irbesartan; Leptin; Male; Microcirculation; Nitric Oxide Synthase; Rats; Receptor, Angiotensin, Type 2; Stomach; Tetrazoles; Triglycerides