Abstract: Described herein is a novel, mitochondrial encoded, open reading frame, that leads to the production of a new mitochondrial peptide. Residing within the ND-Two subunit, a specific small nucleotide polymorphism disrupts expression of this mitochondrial peptide, and is correlated with an increase in obesity and diabetes, particularly in certain ethnic populations. In vitro administration of the peptide increases insulin secretion, decreases fat accumulation and improves glucose uptake in muscle cell. Antibodies generated against the peptide can be used for detecting peptide deficiency, in addition to SNP detection, supporting diagnostic approaches. In vivo studies further revealed that administration of the peptide improves glucose tolerance, thereby providing a new therapeutic avenue for a novel diabetes therapy and decreases bodyweight, thus serving as a novel obesity therapy. Generation of synthetic analogs further enhance or abrogated activity relative to the natural peptide.

Abstract: Described herein is a novel, mitochondrial encoded, open reading frame, that leads to the production of a new mitochondrial peptide. Residing within the ND-Two subunit, a specific small nucleotide polymorphism disrupts expression of this mitochondrial peptide, and is correlated with an increase in obesity and diabetes, particularly in certain ethnic populations. In vitro administration of the peptide increases insulin secretion, decreases fat accumulation and improves glucose uptake in muscle cell. Antibodies generated against the peptide can be used for detecting peptide deficiency, in addition to SNP detection, supporting diagnostic approaches. In vivo studies further revealed that administration of the peptide improves glucose tolerance, thereby providing a new therapeutic avenue for a novel diabetes therapy and decreases bodyweight, thus serving as a novel obesity therapy. Generation of synthetic analogs further enhance or abrogated activity relative to the natural peptide.

Abstract: Described herein is a new mitochondrial peptide. This small peptide is capable of modulating cancer, through a variety of mechanisms including autophagy/apoptosis, reduction of tumor cell viability, inducing inflammatory response in senescent cells and conversion of macrophage cell type. Administration of the peptide, its analogs and derivatives thereof, are likely to be effective treatments for cancer therapy, including generation of synthetic analogs that further enhance or abrogate activity relative to the peptide.

Abstract: Described herein is a novel, mitochondrial encoded, open reading frame, that leads to the production of a new mitochondrial peptide. Residing within the ND-Two subunit, a specific small nucleotide polymorphism disrupts expression of this mitochondrial peptide, and is correlated with an increase in obesity and diabetes, particularly in certain ethnic populations. In vitro administration of the peptide increases insulin secretion, decreases fat accumulation and improves glucose uptake in muscle cell. Antibodies generated against the peptide can be used for detecting peptide deficiency, in addition to SNP detection, supporting diagnostic approaches. In vivo studies further revealed that administration of the peptide improves glucose tolerance, thereby providing a new therapeutic avenue for a novel diabetes therapy and decreases bodyweight, thus serving as a novel obesity therapy. Generation of synthetic analogs further enhance or abrogated activity relative to the natural peptide.

Abstract: The present disclosure provides a method of improvement, preservation, prophylaxis, or inhibition-of-deterioration of a healthspan parameter of a mammalian subject. In exemplary embodiments, the method comprises administering to the subject a composition that comprises an insulin-like growth factor-1 receptor (IGF-1 R) inhibitor, wherein the composition is administered in an amount effective to improve, provide prophylaxis for, or inhibit-the-deterioration of the healthspan parameter.

Abstract: Described herein is a novel, mitochondrial encoded, open reading frame, that leads to the production of a new mitochondrial peptide. Residing within the ND-Two subunit, a specific small nucleotide polymorphism disrupts expression of this mitochondrial peptide, and is correlated with an increase in obesity and diabetes, particularly in certain ethnic populations. In vitro administration of the peptide increases insulin secretion, decreases fat accumulation and improves glucose uptake in muscle cell. Antibodies generated against the peptide can be used for detecting peptide deficiency, in addition to SNP detection, supporting diagnostic approaches. In vivo studies further revealed that administration of the peptide improves glucose tolerance, thereby providing a new therapeutic avenue for a novel diabetes therapy and decreases bodyweight, thus serving as a novel obesity therapy. Generation of synthetic analogs further enhance or abrogated activity relative to the natural peptide.

Abstract: MOTS3 is a novel polypeptide. Methods of treating diseases such as diabetes, obesity, fatty liver, and cancer using MOTS3 and pharmaceutical compositions thereof are disclosed herein.

Abstract: Described herein is a novel, mitochondrial encoded, open reading frame, that leads to the production of a new mitochondrial peptide. Residing within the ND-Two subunit, a specific small nucleotide polymorphism disrupts expression of this mitochondrial peptide, and is correlated with an increase in obesity and diabetes, particularly in certain ethnic populations. In vitro administration of the peptide increases insulin secretion, decreases fat accumulation and improves glucose uptake in muscle cell. Antibodies generated against the peptide can be used for detecting peptide deficiency, in addition to SNP detection, supporting diagnostic approaches. In vivo studies further revealed that administration of the peptide improves glucose tolerance, thereby providing a new therapeutic avenue for a novel diabetes therapy and decreases bodyweight, thus serving as a novel obesity therapy. Generation of synthetic analogs further enhance or abrogated activity relative to the natural peptide.

Abstract: MOTS3 is a novel polypeptide. Methods of treating diseases such as diabetes, obesity, fatty liver, and cancer using MOTS3 and pharmaceutical compositions thereof are disclosed herein.

Abstract: MOTS3 is a novel polypeptide. Methods of treating diseases such as diabetes, obesity, fatty liver, and cancer using MOTS3 and pharmaceutical compositions thereof are disclosed herein.

Abstract: MOTS3 is a novel polypeptide. Methods of treating diseases such as diabetes, obesity, fatty liver, and cancer using MOTS3 and pharmaceutical compositions thereof are disclosed herein.

Abstract: MOTS3 is a novel polypeptide. Methods of treating diseases such as diabetes, obesity, fatty liver, and cancer using MOTS3 and pharmaceutical compositions thereof are disclosed herein.

Abstract: Novel peptides referred to as small humanin-like peptides (SHLPs) are provided herein along with nucleic acids encoding SHLPs and probes that selectively bind SHLPs. SHLPs have wide-ranging activity, including neuroprotective activity, anticancer activity, and cell survival activity. Also provided herein are therapeutic methods comprising administering an effective amount of an SHLP to a subject in need of treatment.

Abstract: The present invention is based on the discovery that Humanin and humanin analogues protect pancreatic beta cells in vitro and in vivo from apoptosis. Accordingly, humanin and its analogues are useful for preventing and treating diabetes and promoting beta cell survival in a number of applications.

Abstract: Novel peptides referred to as small humanin-like peptides (SHLPs) are provided herein along with nucleic acids encoding SHLPs and probes that selectively bind SHLPs. SHLPs have wide-ranging activity, including neuroprotective activity, anticancer activity, and cell survival activity. Also provided herein are therapeutic methods comprising administering an effective amount of an SHLP to a subject in need of treatment.

Abstract: The present invention is directed to methods and compositions for preventing or reducing atherosclerotic lesions and plaques. Specifically, the instant invention provides methods for using humanin and its analogues to prevent or reduce the formation of atherosclerotic plaques. Also provided are methods of using humanin and its analogues to improve the survival of endothelial cells, particularly aortic endothelial cells.

Abstract: Provided are methods of using humanin and humanin analogs to treat a mammal exhibiting or at risk for insulin resistance, increase insulin sensitivity in a mammal exhibiting or at risk for insulin resistance, treat type-2 diabetes mellitus, metabolic syndrome, and neurodegeneration, treat and prevent myocardial injury, and determine longevity.

Abstract: Provided are methods of using humanin and humanin analogs to treat a mammal exhibiting or at risk for insulin resistance, increase insulin sensitivity in a mammal exhibiting or at risk for insulin resistance, treat type-2 diabetes mellitus, metabolic syndrome, and neurodegeneration, treat and prevent myocardial injury, and determine longevity.

Abstract: The present invention is based on the discovery that Humanin and humanin analogues protect pancreatic beta cells in vitro and in vivo from apoptosis. Accordingly, humanin and its analogues are useful for preventing and treating diabetes and promoting beta cell survival in a number of applications.

Abstract: The present invention is based on the discovery that Humanin and humanin analogues protect pancreatic beta cells in vitro and in vivo from apoptosis. Accordingly, humanin and its analogues are useful for preventing and treating diabetes and promoting beta cell survival in a number of applications.