Counterregulatory responses of healthy cats to insulin- induced-hypoglycemia.

IF 4.2 2区 医学 Q1 ENDOCRINOLOGY & METABOLISM
Jocelyn Mott, Christopher Adin, Chiquitha Crews, Marc Evan Salute, Antonio Maria Tardo, Lauren Porter, Alisa Berg, Chen Gilor
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引用次数: 0

Abstract

In health, insulin-induced-hypoglycemia (IIH) activates counterregulatory hormones responses and parasympathetic (PS) and sympathoadrenal systems which leads to increased glucagon secretion. In diabetes mellitus, these responses are impaired, resulting in greater severity and delayed recovery from hypoglycemia. These counterregulatory responses in health and disease have been documented in humans, rodents, and dogs, but not yet in cats. The aim of this study was to describe and quantify glucagon, PS and cortisol responses in healthy purpose bred cats at increasing levels of IIH. Glucagon, cortisol, and pancreatic polypeptide (PP) were measured at euglycemia and during stepped hyperinsulinemic-hypoglycemic clamps at two levels of glycemia: moderate hypoglycemia (blood glucose [BG] ~60 mg/dL) and severe hypoglycemia (BG ~45 mg/dL). At moderate hypoglycemia, a cortisol response occurred. At moderate hypoglycemia there was no change in PP and glucagon from baseline. With severe hypoglycemia, both glucagon and PP concentrations decreased from baseline and were not supportive of glucagon and parasympathetic activation in response to IIH. While cortisol increases during IIH, the counterregulatory response to IIH in healthy cats differs from other species, in that glucagon and PS responses were not detected. Moreover, in face of constant inhibition by IIH, glucagon secretion seems dependent on glucose, decreasing when glucose infusion rates were decreased. Understanding counterregulatory responses to hypoglycemia in healthy cats is the first step to exploring how diabetes might impair these responses in cats, as seen in other species.

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来源期刊
CiteScore
9.80
自引率
0.00%
发文量
98
审稿时长
1 months
期刊介绍: The American Journal of Physiology-Endocrinology and Metabolism publishes original, mechanistic studies on the physiology of endocrine and metabolic systems. Physiological, cellular, and molecular studies in whole animals or humans will be considered. Specific themes include, but are not limited to, mechanisms of hormone and growth factor action; hormonal and nutritional regulation of metabolism, inflammation, microbiome and energy balance; integrative organ cross talk; paracrine and autocrine control of endocrine cells; function and activation of hormone receptors; endocrine or metabolic control of channels, transporters, and membrane function; temporal analysis of hormone secretion and metabolism; and mathematical/kinetic modeling of metabolism. Novel molecular, immunological, or biophysical studies of hormone action are also welcome.
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