It is increasingly accepted that the metabolic future of an individual can be programmed as early as at developmental stages. For instance, offspring of diabetic mothers have a greater risk of becoming obese and diabetic later in life. Animal studies have demonstrated that hyperinsulinemia and/or hyperglycemia during perinatal life permanently impair the organization and long-term function of hypothalamic networks that control appetite and glucose homeostasis. This review summarizes the main findings regarding the key regulatory roles of perinatal insulin and glucose levels on hypothalamic development and on long-term programming of metabolic diseases reported in different rodent models.
It is increasingly accepted that the metabolic future of an individual can be programmed as early as at developmental stages. For instance, offspring of diabetic mothers have a greater risk of becoming obese and diabetic later in life. Animal studies have demonstrated that hyperinsulinemia and/or hyperglycemia during perinatal life permanently impair the organization and long-term function of hypothalamic networks that control appetite and glucose homeostasis. This review summarizes the main findings regarding the key regulatory roles of perinatal insulin and glucose levels on hypothalamic development and on long-term programming of metabolic diseases reported in different rodent models.
It is increasingly accepted that the metabolic future of an individual can be programmed as early as at developmental stages. For instance, offspring of diabetic mothers have a greater risk of becoming obese and diabetic later in life. Animal studies have demonstrated that hyperinsulinemia and/or hyperglycemia during perinatal life permanently impair the organization and long-term function of hypothalamic networks that control appetite and glucose homeostasis. This review summarizes the main findings regarding the key regulatory roles of perinatal insulin and glucose levels on hypothalamic development and on long-term programming of metabolic diseases reported in different rodent models.
It is increasingly accepted that the metabolic future of an individual can be programmed as early as at developmental stages. For instance, offspring of diabetic mothers have a greater risk of becoming obese and diabetic later in life. Animal studies have demonstrated that hyperinsulinemia and/or hyperglycemia during perinatal life permanently impair the organization and long-term function of hypothalamic networks that control appetite and glucose homeostasis. This review summarizes the main findings regarding the key regulatory roles of perinatal insulin and glucose levels on hypothalamic development and on long-term programming of metabolic diseases reported in different rodent models.
It is increasingly accepted that the metabolic future of an individual can be programmed as early as at developmental stages. For instance, offspring of diabetic mothers have a greater risk of becoming obese and diabetic later in life. Animal studies have demonstrated that hyperinsulinemia and/or hyperglycemia during perinatal life permanently impair the organization and long-term function of hypothalamic networks that control appetite and glucose homeostasis. This review summarizes the main findings regarding the key regulatory roles of perinatal insulin and glucose levels on hypothalamic development and on long-term programming of metabolic diseases reported in different rodent models.
It is increasingly accepted that the metabolic future of an individual can be programmed as early as at developmental stages. For instance, offspring of diabetic mothers have a greater risk of becoming obese and diabetic later in life. Animal studies have demonstrated that hyperinsulinemia and/or hyperglycemia during perinatal life permanently impair the organization and long-term function of hypothalamic networks that control appetite and glucose homeostasis. This review summarizes the main findings regarding the key regulatory roles of perinatal insulin and glucose levels on hypothalamic development and on long-term programming of metabolic diseases reported in different rodent models.
It is increasingly accepted that the metabolic future of an individual can be programmed as early as at developmental stages. For instance, offspring of diabetic mothers have a greater risk of becoming obese and diabetic later in life. Animal studies have demonstrated that hyperinsulinemia and/or hyperglycemia during perinatal life permanently impair the organization and long-term function of hypothalamic networks that control appetite and glucose homeostasis. This review summarizes the main findings regarding the key regulatory roles of perinatal insulin and glucose levels on hypothalamic development and on long-term programming of metabolic diseases reported in different rodent models.
It is increasingly accepted that the metabolic future of an individual can be programmed as early as at developmental stages. For instance, offspring of diabetic mothers have a greater risk of becoming obese and diabetic later in life. Animal studies have demonstrated that hyperinsulinemia and/or hyperglycemia during perinatal life permanently impair the organization and long-term function of hypothalamic networks that control appetite and glucose homeostasis. This review summarizes the main findings regarding the key regulatory roles of perinatal insulin and glucose levels on hypothalamic development and on long-term programming of metabolic diseases reported in different rodent models.
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