Purpose: Gastric dysmotility has been reported in patients with long-standing diabetes mellitus (DM). Some patients with DM are diagnosed as diabetes gastroparesis and have several upper gastrointestinal (GI) symptoms such as appetite loss and abdominal pain. This study aimed to identify the relationship between gastric motility and upper GI symptoms in patients with long-standing DM. Method: This study was conducted among 23 patients with DM and 15 healthy controls. All the patients with DM were receiving insulin treatment and had at least one history of incidence of diabetic nephropathy, retinopathy or neuropathy. Gastric motility was evaluated using electrogastrography (EGG) and gastric emptying using the ¹³C-acetic acid breath test. The most severe upper gastrointestinal symptoms were assessed in all patients. Results: Compared to healthy controls, patients with long-standing DM showed a significantly lower percentage of normogastria at the postprandial state with a lower power ratio in EGG. Gastric emptying was significantly delayed in patients with DM in the overall analysis. Sixteen patients with DM (69.6%) demonstrated abnormalities in either gastric myoelectrical activity or gastric emptying. Among patients with abnormal EGG or delayed gastric emptying, 12 had some GI symptoms, compared with 3 patients with normal gastric motility. No significant correlation was observed between the gastric emptying parameters and HbA1c values. Conclusion: Patients with long-standing DM showed gastric dysmotility, including impaired gastric myoelectrical activity and delayed gastric emptying. Gastric dysmotility appears to be closely correlated with upper GI symptoms in patients with long-standing DM.

This review highlights molecular mechanisms of anti-inflammatory and protective effects of the nuclear transcription factor, peroxisome proliferator-activated receptor γ (PPARγ) in vascular tissue. PPARγ is an ubiquitously expressed nuclear factor, and well-studied in adipose tissue and inflammatory cells. Additionally, beneficial effects of vascular PPARγ’s on atherosclerosis and vascular remodeling/dysfunction have been reported although the detailed mechanism remains to be completely elucidated. Clinical and basic studies have shown that the synthetic PPARγ ligands, thiazolidinediones (TZDs), have protective effects against cardiovascular diseases such as atherosclerosis. Recent studies utilizing genetic tools suggested that those protective effects of TZDs on cardiovascular diseases are not due to a consequence of improvement of insulin resistance, but may be due to a direct effect on PPARγ’s in vascular endothelial and smooth muscle cells. In this review, we discuss proposed mechanisms by which the vascular PPARγ regulates vascular inflammation and remodeling/dysfunction especially in smooth muscle cells.

Pompe disease is a lysosomal storage disease caused by mutations within the GAA gene, which encodes acid α-glucosidase (GAA)—an enzyme necessary for lysosomal glycogen degradation. A lack of GAA results in an accumulation of glycogen in cardiac and skeletal muscle, as well as in motor neurons. The only FDA approved treatment for Pompe disease—an enzyme replacement therapy (ERT)—increases survival of patients, but has unmasked previously unrecognized clinical manifestations of Pompe disease. These clinical signs and symptoms include tracheo-bronchomalacia, vascular aneurysms, and gastro-intestinal discomfort. Together, these previously unrecognized pathologies indicate that GAA-deficiency impacts smooth muscle in addition to skeletal and cardiac muscle. Thus, we sought to characterize smooth muscle pathology in the airway, vascular, gastrointestinal, and genitourinary in the Gaa^−/− mouse model. Increased levels of glycogen were present in smooth muscle cells of the aorta, trachea, esophagus, stomach, and bladder of Gaa^−/− mice, compared to wild type mice. In addition, there was an increased abundance of both lysosome membrane protein (LAMP1) and autophagosome membrane protein (LC3) indicating vacuolar accumulation in several tissues. Taken together, we show that GAA deficiency results in subsequent pathology in smooth muscle cells, which may lead to life-threatening complications if not properly treated.

The characteristic mechanical activities of the smooth muscles found in all organs of the body are highly variable and depend mainly on the spatial arrangement of the muscle cells and the stroma: mass, orientation, relationships, links, constraints, which are deployed in various configurations. These structural features are examined here for their mechanical relevance, in light and electron microscopic views of several muscles of viscera and blood vessels, in a selection of mammalian species. Smooth muscles are incompressible and therefore maintain constant volume. They do not have available space and any movement of a part requires displacement of another part. Most of them have no terminations or points of attachment, and in hollow organs such as intestines, blood vessels and uro-genital tract they usually form structures closed onto themselves, such as rings or bag-like containers In these situations, changes in the size of the lumen is achieved very efficiently by a concentric inward enlargement that accompanies muscle contraction. The longitudinal arrangement of collagen blocks an elongation of small blood vessels upon contraction, further enhancing the efficiency of lumen reduction. In other muscles, links between layers and special arrangements of the stroma allow both shortening and elongation of a tubular organ to occur. The mechanics of smooth muscles has many characteristic features (some unique, some shared with those of hydrostats, some at variance with other muscles) and histological data are a contribution to our understanding of these properties.

Intestinal spasms are violent contractions that occur in the intestine, which cause discomfort to people who have them. Medicinal plants are widely used in traditional Moroccan medicine to treat these problems, among these being Artemisia campestris L. This study aims to evaluate the relaxant and antispasmodic effects of an aqueous extract of this plant (ACAE). It was performed in vitro on isolated segments of both isolated rat and rabbit jejunum mounted in an organ bath and tension recordings made via an isotonic transducer. ACAE caused a myorelaxant effect on baseline rabbit jejunum contractions in a dose-dependent and reversible manner with an IC₅₀ of 1.52 ± 0.12 mg/ml. This extract would not act via adrenergic receptors pathway. On the other hand, the extract caused a dose-dependent relaxation of the jejunum tone in rat jejenum segments pre-contracted with either Carbachol (CCh; 10⁻⁶ M) or high K⁺ (KCl 75 mM) with an IC₅₀ = 0.49 ± 0.02 mg/ml and 0.36 ± 0.02 mg/ml respectively. In the presence of different doses of the extract, the maximum response to CCh and CaCl₂ was significantly reduced. This demonstrates that ACAE acts on both muscarinic receptors and voltage-dependent calcium channels. Thus, the plant extract acted on both muscarinic and nicotinic receptors and acts on the guanylate cyclase pathway, but not the nitric oxide pathway. These results indicate the mechanism by which Artemisia campestris L. acts as an effective antispasmodic agent in traditional Moroccan medicine.