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Gi and pancreatic device for treating obesity and diabetes

USPTO Application #: 20070016262
Title: Gi and pancreatic device for treating obesity and diabetes
Abstract: A method is provided, including placing first and second electrodes at respective first and second sites of a duodenum of a subject, and activating the electrodes to increase a blood insulin level of the subject. Other embodiments are also described. (end of abstract)
Agent: Darby & Darby P.C. - New York, NY, US
Inventors: Yossi Gross, Jacob Benarie, Radwin Khawaled, Ruth Alon
USPTO Applicaton #: 20070016262 - Class: 607040000 (USPTO)
Related Patent Categories: Surgery: Light, Thermal, And Electrical Application, Light, Thermal, And Electrical Application, Electrical Therapeutic Systems, Stimulating Bladder Or Gastrointestinal Tract
The Patent Description & Claims data below is from USPTO Patent Application 20070016262.
Brief Patent Description - Full Patent Description - Patent Application Claims  monitor keywords

CROSS-REFERENCES TO RELATED APPLICATIONS

[0001] The present patent application claims the benefit of:

[0002] (a) U.S. Provisional Patent Application 60/699,442 to Alon and Gross, filed Jul. 13, 2005, entitled, "GI and pancreatic device for treating obesity and diabetes," and

[0003] (b) US Provisional Patent Application 60/720,951 to Alon and Gross, filed Sep. 26, 2005, entitled, "GI and pancreatic device for treating obesity and diabetes."

[0004] Each of these applications is incorporated herein by reference.

FIELD OF THE INVENTION

[0005] The present invention relates generally to treating obesity and diabetes, and specifically to methods and apparatus that treat obesity and diabetes from within the gastrointestinal tract and pancreas.

BACKGROUND OF THE INVENTION

[0006] Obesity and diabetes are frequently linked diseases, although some patients with one condition do not suffer from the other. The multiple causes of obesity are a subject of ongoing research. Insulin resistance and beta-cell dysfunction are two important factors contributing to the development of diabetes. The relationship between these two factors has been extensively studied, as has the role of obesity in diabetes. In particular, it has been widely observed that obesity is a principal cause of insulin resistance. Most patients who develop type II diabetes are obese.

[0007] As described in an article by Michael Gershon entitled, "The enteric nervous system: A second brain" (Hospital Practice, July, 1999), which is incorporated herein by reference, the enteric nervous system (ENS) is a portion of the autonomic nervous system which consists of two layers. The first layer is called the myenteric (Auerbach's) plexus, and lies between the layers of circular and longitudinal muscle lining the gut wall. The second layer is called the submucosal plexus, and lies between the layer of circular muscle and the submucosa. The myenteric plexus contains neurons responsible for motility and for mediating the enzyme output of adjacent organs. The smaller, submucosal (Meissner's) plexus contains sensory cells that communicate with the neurons of the myenteric plexus, as well as motor fibers that stimulate secretion from epithelial crypt cells into the gut lumen. Electrical coupling between smooth muscle cells enables signals to rapidly alter the membrane potential of even those cells that have no direct contact with neurons and ensures that large regions of bowel--rather than small groups of muscle cells--will respond to nerve stimulation.

[0008] PCT Patent Publication WO 2005/007232 to Ben-Haim et al., which is incorporated herein by reference, describes a method and apparatus for treating a subject. An electrical signal is applied to at least one stomach site of the subject. The electrical signal is configured to reduce a rise in a blood glucose level of the subject, in order to treat the subject. A colonic stimulation system is also described, comprising a control unit and one or more electrodes, which are adapted to be applied to respective sites in a vicinity of a colon or a distal small intestine of a patient. The control unit drives the electrodes to apply electrical signals to the sites, and configures the signals to stimulate L-cells or other target tissue, which, responsive to such stimulation, increase secretion of glucagon-like-peptide-1 (GLP-1). Such secretion of GLP-1 is described as generally improving glycemic control of the patient, and therefore serving to treat patients suffering from insulin-resistance-related conditions, such as obesity, NIDDM, heart disease, and hypertension, or healthy patients considered at risk for such conditions. For some applications, the colonic stimulation system further comprises an eating detection unit, and the control unit is configured to drive the electrodes to apply the signals responsive to a detection of eating.

[0009] U.S. Pat. No. 6,091,992 to Bourgeois et al., which is incorporated herein by reference, describes a method and apparatus for providing electrical stimulation to the gastrointestinal tract. The apparatus features an implantable pulse generator which may be coupled to the gastric system through one or more medical electrical leads. In the preferred embodiment the leads couple to the circular layer of the stomach. In one embodiment, the implantable system includes a hermetically sealed implantable pulse generator, the pulse generator emitting a first type of electrical stimulation at a first rate and a second type of electrical stimulation at a second rate.

[0010] The following articles, which are incorporated herein by reference, may be of interest:

[0011] U.S. Pat. No. 6,191,102 to DiMarchi et al.

[0012] Todd J F et al., "Glucagon-like peptide-1 (GLP-1): a trial of treatment in non-insulin-dependent diabetes mellitus," Eur J Clin Invest 27(6):533-6 (1997)

[0013] Gutniak M K et al., "Subcutaneous injection of the incretin hormone glucagon-like peptide 1 abolishes postprandial glycemia in NIDDM," Diabetes Care 17(9) :1039-44 (1994)

[0014] Robertson M D et al., "The influence of the colon on postprandial glucagon-like peptide 1 (7-36) amide concentration in man," J Endocrinol 161(1):25-31 (1999)

[0015] Schirra J et al., "Mechanisms of the antidiabetic action of subcutaneous glucagon-like peptide-1 (7-36) amide in non-insulin dependent diabetes mellitus," J Endocrinol 156(1):177-86 (1998)

[0016] Todd J F et al., "Subcutaneous glucagon-like peptide-1 improves postprandial glycaemic control over a 3-week period in patients with early type 2 diabetes," Clin Sci (Lond) 95(3):325-9 (1998)

[0017] Vilsboll T et al., "Reduced postprandial concentrations of intact biologically active glucagon-like peptide 1 in type 2 diabetic patients," Diabetes 50(3):609-13 (2001).

[0018] U.S. Pat. No. 6,322,560 to Garbagnati et al., which is incorporated herein by reference, describes a catheter for the treatment of tumors by hyperthermia induced by radiofrequency or other energy. The catheter comprises a tubular body having a cooled metal plate capable of acting as an active electrode. One application described is the treatment of pancreatic tumors by introducing the catheter through the main pancreatic duct by endoscopy or during surgery.

[0019] U.S. Pat. No. 6,575,969 to Rittman, III et al., which is incorporated herein by reference, describes a fluid-cooled (perfusion-cooled) high-frequency electrode. In one embodiment, the electrode comprises a "stint," a balloon, or a condom-like structure that can be inserted into the pancreatic duct, and by appropriate cooling in conjunction with RF heating, it can "throw" the heat into a pancreatic tumor while sparing the structure of the duct to preserve normal processing of biological fluids.

[0020] U.S. Pat. No. 5,188,104 to Wernicke et al., which is incorporated herein by reference, describes a method for treating patients with compulsive eating disorders, including detecting a preselected event indicative of an imminent need for treatment of the specific eating disorder of interest, and responding to the detected occurrence of the preselected event by applying a predetermined stimulating signal to the patient's vagus nerve appropriate to alleviate the effect of the eating disorder of interest. For example, the preselected event may be a specified level of food consumption by the patient within a set interval of time, or the commencement of a customary mealtime according to the patient's circadian cycle, or the passage of each of a sequence of preset intervals of time, or the patient's own recognition of the need for treatment by voluntarily initiating the application of the stimulating signal to the vagus nerve. In cases in which the disorder is compulsive eating to excess, the stimulating signal is described as being predetermined to produce a sensation of satiety in the patient.

[0021] US Patent Application Publication 2005/0021101 to Chen et al., which is incorporated herein by reference, describes a method for regulating gastrointestinal action in a subject using a stimulatory electrode and a sensor to provide retrograde feedback control of electrical stimulation to the GI tract. Also described is a method for reducing weight in a subject, using a stimulatory electrode and a sensor to provide retrograde feedback control of electrical stimulation to the stomach. Further described is a method for providing electrical field stimulation to a gastrointestinal organ, as well as a method of providing an electrical potential gradient in a gastrointestinal organ. Further described is a method for stimulating the vagus nerve of a subject, by positioning a stimulatory electrode in a gastrointestinal organ of the subject. Additionally described is a method of placing a device in the gastrointestinal tract or wall of a subject from the exterior of the subject, using a needle to insert the device.

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