IP Library Patent Application 11884298
Patent Application
App. No. 11/884,298

Modulation of Hypothalamic Atp-Sensitive Potassium Channels

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Patent No.
US None
App. No.
11/884,298
Abstract

Provided are methods of increasing K ATP activity in the hypothalamus of a mammal, methods of reducing glucose production and peripheral blood glucose levels in a mammal, methods of inhibiting gluconeogenesis in the liver of a mammal, and methods of increasing glucose production and peripheral blood glucose levels in a mammal.

Claims (23)

1 - 27 . (canceled)

28 . A method of reducing peripheral blood glucose levels, glucose production, gluconeogenesis in the liver, serum triglycerides levels, or serum very low density lipoprotein (VLDL) levels, in a mammal, the method comprising administering a K ATP channel activator to the hypothalamus of the mammal in an amount effective to reduce peripheral blood glucose levels, glucose production, gluconeogenesis in the liver, serum triglycerides levels, or serum very low density lipoprotein (VLDL) levels, in the mammal.

29 . A method of increasing K ATP activity in the hypothalamus of a mammal, the method comprising bringing a K ATP channel activator into contact with the hypothalamus of the mammal in an amount effective to increase K ATP activity in the hypothalamus.

30 . The method of claim 1 , wherein the mammal has at least one condition or disorder selected from the group consisting of obesity, type 2 diabetes, type 1 diabetes, hyperglycemia, insulin resistance, glucose intolerance, leptin resistance, metabolic syndrome, gonadotropin deficiency, amenorrhea, heart failure, ischemia, coronary heart disease, familial lipoprotein lipase deficiency, hypopituitarism, hyperlipidemia, hypertriglyceridemia, hyperVLDLemia, atherosclerosis, hypercholesterolemia, hypertension and polycystic ovary syndrome, and said condition or disorder is treated by the K ATP channel activator.

31 . The method of claim 1 , wherein the K ATP channel activator is a cyanoguanidine or a benzothiazine 1,1-dioxide.

32 . The method of any claim 1 , wherein the K ATP channel activator is selected from the group consisting of diazoxide, pinacidil, (−)-cromakalim, aprikalim, bimakalim, emakalim, nicordandil, NNC 55-0118, NN414, EMD55387, HOE234, KRN2391, minoxidil sulfate, P1060, P1075, RP49356, RP66471, and combinations thereof.

33 . The method of claim 1 , wherein the K ATP channel activator is diazoxide.

34 . The method of claim 1 , wherein the K ATP channel activator is formulated in a pharmaceutical composition that enhances the ability of the activator to cross the blood-brain barrier of the mammal.

35 . The method of claim 1 , wherein the K ATP channel activator is administered in a manner that permits the activator to cross the blood-brain barrier of the mammal.

36 . The method of claim 1 , wherein the K ATP channel activator is administered directly to the brain of the mammal.

37 . The method of claim 1 , wherein the mammal is a human.

38 . A method of increasing glucose production in a mammal, the method comprising administering a K ATP channel inhibitor to the hypothalamus of the mammal in an amount effective to increase glucose production in the mammal.

39 . The method of claim 38 , wherein the K ATP channel inhibitor is a sulfonylurea.

40 . The method of claim 38 , wherein the K ATP channel inhibitor is selected from the group consisting of glibenclamide, phentolamine, ciclazindol, lidocaine, glipizide, U37883A, tolbutamide, and combinations thereof.

41 . The method of claim 38 , wherein the K ATP channel inhibitor is formulated in a pharmaceutical composition that enhances the ability of the inhibitor to cross the blood-brain barrier of the mammal.

42 . The method of claim 38 , wherein the K ATP channel inhibitor is administered in a manner that permits the activator to cross the blood-brain barrier of the mammal.

43 . The method of claim 38 , wherein the K ATP inhibitor is administered directly to the brain of the mammal.

44 . The method of claim 38 , wherein the mammal is a human.

45 . The method of claim 38 , wherein the mammal is undergoing a treatment that causes insufficient food intake or glucose production.

46 . The method of claim 45 , wherein the treatment is cancer chemotherapy.

47 . The method of claim 38 , wherein the mammal has a viral infection that causes insufficient glucose production.

48 . The method of claim 47 , wherein the mammal is a human and the infection is with HIV-1.

49 . The method of claim 38 , wherein the mammal is hypoglycemic.

Assignments (4)
CHANGE OF NAME Recorded Oct 20, 2015
From: COM AFFILIATION, INC.
To: ALBERT EINSTEIN COLLEGE OF MEDICINE, INC.
Reel/Frame 036900/0190 →
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Oct 16, 2015
From: ALBERT EINSTEIN COLLEGE OF MEDICINE OF YESHIVA UNIVERSITY
To: COM AFFILIATION, INC.
Reel/Frame 036877/0835 →
GOVERNMENT INTEREST AGREEMENT Recorded Jul 23, 2015
From: ALBERT EINSTEIN COLLEGE OF MEDICINE OF YESHIVA UNIVERSITY
To: NATIONAL INSTITUTES OF HEALTH
Reel/Frame 036160/0899 →
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Jun 11, 2008
From: ROSSETTI, LUCIANO; POCAI, ALESSANDRO
To: ALBERT EINSTEIN COLLEGE OF MEDICINE OF YESHIVA UNIVERSITY
Reel/Frame 021103/0582 →