2017 International Congress of Diabetes and Metabolism

S4 Insulin action/molecular metabolism : Therapeutic targets in skeletal muscle energy metabolism: Friday 29 September 09:00~11:00 | Place: Emerald Hall A
Chairman: Ki-Up Lee, Kyoil Suh

- Therapeutic targets in skeletal muscle energy metabolism Energy metabolism in skeletal muscle has received intensive attention with a growing list of myokines. In this session, recent advance in muscle physiology with a particular emphasis on therapeutic targets will be reviewed. Professor Lee HY (Gachon Univ. Incheon) will present a new data on mitochondrial uncoupler in skeletal muscle. Professor Chang JS (Pennington Biomedical Research Center, Baton Louge) will show new functions of NT-PGC1 in skeletal muscle as well as adipose tissues. Professor Ko YG (Korea University, Seoul) will present new data on the therapeutic role of MG53-IRS-1 Interaction Disruptor for insulin resistance. Finally, Professor Kim JK (University of Massachusetts Medical School, Worcester) will address the therapeutic role of anti-inflammatory cytokine in skeletal muscle, including IL-10, to control insulin resistance. Please join us at this up-to-date muscle physiology/insulin action session to get a therapeutic implication for insulin resistance.

	Hui-Young Lee Gachon University, Korea	S4-1 A mitochondrial uncoupler against muscle insulin resistance and energetics
	Ji Suk Chang Pennington Biomedical Research Center, USA	S4-2 NT-PGC-1α in brown fat and skeletal muscle energy metabolism
	Young-Gyu Ko Korea University, Korea	S4-3 MG53-IRS-1 (mitsugumin 53-insulin receptor substrate-1) interaction disruptor sensitizes insulin signaling in skeletal muscle
	Jason K. Kim University of Massachusetts Medical School, USA	S4-4 Therapeutic role of anti-inflammatory cytokine to treat insulin resistance in obesity and aging

S5 Islet biology & insulin secretion1 : Mechanism of beta cell failure: Friday 29 September 09:00~11:00| Place: Emerald Hall B
Chairman: Kwang-Won Kim, Yu-Bae Ahn

- Mechanism of beta cell failure Although the progression of type 2 diabetes initiates with the development of insulin resistance, hyperglycemia does not develop as long as pancreatic -cells compensate insulin resistance. Thus, -cell failure along with insulin resistance is an essential feature of type 2 diabetes. In this session, four outstanding speakers will share their recent works to explain how -cell failure develops. Prof. Kyu Chang Won and Prof. Ki-Ho Song will talk about how glucotoxicity and fibrosis contribute to the development of -cell failure. Prof. Domenico Accili will talk about -cell dedifferentiation. Prof. Seung Kim will introduce his recent work with human islet and it implication for diabetes.

	Kyu Chang Won Yeungnam University, Korea	S5-1 Glucotoxicity and CD36 related beta cell dysfunction
	Ki-Ho Song The Catholic University of Korea, Korea	S5-2 Islet fibrosis
	Domenico Accili Columbia University, USA	S5-3 When beta cells fail: lessons from dedifferentiation
	Seung Kim Stanford University, USA	S5-4 Age-dependent human beta-cell proliferation induced by GLP-1 and calcineurin signaling

S10 Islet biology & insulin secretion 2 : Clinical focus on glucagon: α-cell as a companion of β-cell: Friday 29 September 16:00~18:00| Place: Emerald Hall B
Chairman: Sung-Hee Ihm, Ki-Ho Song

- Clinical focus on glucagon Type 2 diabetes consists of an array of dysfunctions and resulting from the combination of multiple pathophysiology. Among them, hyperglucagonemia and aberrant glucagon action have been implicated in contributing to hyperglycemia in diabetic patients. In this session, we will address the glucagon secretion and action in diabetic patients from physiology to treatment strategies. At opening the session, Professor Filip Knop will discuss about the pathophysiology of glucagon secretion and action in diabetic patients. And then, Professor Sung Hwan Suh will discuss the recent anti-diabetic drug therapy that reduce glucagon secretion and its clinical implications and limitations. Professor Jin hwa Kim will introduce the new targeted therapy antagonizing glucagon action and discuss whether glucagon antagonism could be a viable anti-diabetic approach. Finally, Professor Jae Hyoung Cho will introduce the new therapeutic target toward glucagon receptor, especially about the development and clinical trials of multi-agonist. I hope that this session has helped to understand the bidirectional relationship between insulin and glucagon and the investigation of glucagon-based therapeutic approaches

	Filip K. Knop University of Copenhagen, Denmark	S10-1 Physiology of glucagon and its role in diabetes
	Sunghwan Suh Dong-A University, Korea	S10-2 Therapeutic strategy to reduce glucagon secretion
	Jin Hwa Kim Chosun University, Korea	S10-3 Therapeutic strategy to antagonize glucagon action
	Jae Hyoung Cho The Catholic University of Korea, Korea	S10-4 Targeting glucagon receptor family: emerging role of multiagonist