Functional abnormalities of islets of Langerhans of obese hyperglycemic mouse.

Lavine, Robert L.; Voyles, Nancy R.; Perrino, P V; Recant, Lillian

doi:10.1152/ajpendo.1977.233.2.e86

Cited by 20 publications

(20 citation statements)

References 6 publications

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“…The mechanisms involved in the maintenance of a high glycogen content in livers of obese mice during starvation are however unclear. A decrease in the cyclic AMP content of livers of starved obese mice [22] might be of relevance.…”

Section: Discussionmentioning

confidence: 99%

Increased concentration of fructose 2,6‐bisphosphate in livers of genetically obese mice

Hue

Werve

1982

FEBS Letters

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Section: Discussionmentioning

confidence: 99%

Increased concentration of fructose 2,6‐bisphosphate in livers of genetically obese mice

Hue

Werve

1982

FEBS Letters

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“…Other metabolic alterations include hyperlipidemia, dysregulated body temperature, and reduced physical activity [137]. The pancreatic b-cell mass is dramatically increased in ob/ob mice, and insulin secretion is maintained [138,139], thus the resulting diabetes is not severe. In contrast, ob/ob mice in the C57BL/ Ks background develop a more severe type of diabetes characterized by the regression of islets [140].…”

Section: Rodent Models Of Type 2 Diabetes Mellitusmentioning

confidence: 99%

Differential control of muscle mass in type 1 and type 2 diabetes mellitus

Sala

Zorzano

2015

Cell. Mol. Life Sci.

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Diabetes mellitus--whether driven by insulin deficiency or insulin resistance--causes major alterations in muscle metabolism. These alterations have an impact on nutrient handling, including the metabolism of glucose, lipids, and amino acids, and also on muscle mass and strength. However, the ways in which the distinct forms of diabetes affect muscle mass differ greatly. The most common forms of diabetes mellitus are type 1 and type 2. Thus, whereas type 1 diabetic subjects without insulin treatment display a dramatic loss of muscle, most type 2 diabetic subjects show no changes or even an increase in muscle mass. However, the most commonly used rodent models of type 2 diabetes are characterized by muscle atrophy and do not mimic the features of the disease in humans in terms of muscle mass. In this review, we analyze the processes that are differentially regulated under these forms of diabetes and propose regulatory mechanisms to explain them.

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“…The ob/ob mice have increased islet cell mass, due primarily to islet cell hyperplasia and hypertrophy (26,49). To exclude the possibility that the reduced pancreatic function of Ghsr Ϫ/Ϫ :ob/ob mice was due to reduced islet cell mass, we performed histological examinations by H & E staining to evaluate islet size.…”

Section: E428 Ghrelin Receptor and Glucose Homeostasismentioning

confidence: 99%

Ablation of ghrelin receptor in leptin-deficient ob/ob mice has paradoxical effects on glucose homeostasis when compared with ablation of ghrelin in ob/ob mice

Lin

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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The orexigenic hormone ghrelin is important in diabetes because it has an inhibitory effect on insulin secretion. Ghrelin ablation in leptin-deficient ob/ob (Ghrelin(-/-):ob/ob) mice increases insulin secretion and improves hyperglycemia. The physiologically relevant ghrelin receptor is the growth hormone secretagogue receptor (GHS-R), and GHS-R antagonists are thought to be an effective strategy for treating diabetes. However, since some of ghrelin's effects are independent of GHS-R, we have utilized genetic approaches to determine whether ghrelin's effect on insulin secretion is mediated through GHS-R and whether GHS-R antagonism indeed inhibits insulin secretion. We investigated the effects of GHS-R on glucose homeostasis in Ghsr-ablated ob/ob mice (Ghsr(-/-):ob/ob). Ghsr ablation did not rescue the hyperphagia, obesity, or insulin resistance of ob/ob mice. Surprisingly, Ghsr ablation worsened the hyperglycemia, decreased insulin, and impaired glucose tolerance. Consistently, Ghsr ablation in ob/ob mice upregulated negative β-cell regulators (such as UCP-2, SREBP-1c, ChREBP, and MIF-1) and downregulated positive β-cell regulators (such as HIF-1α, FGF-21, and PDX-1) in whole pancreas; this suggests that Ghsr ablation impairs pancreatic β-cell function in leptin deficiency. Of note, Ghsr ablation in ob/ob mice did not affect the islet size; the average islet size of Ghsr(-/-):ob/ob mice is similar to that of ob/ob mice. In summary, because Ghsr ablation in leptin deficiency impairs insulin secretion and worsens hyperglycemia, this suggests that GHS-R antagonists may actually aggravate diabetes under certain conditions. The paradoxical effects of ghrelin ablation and Ghsr ablation in ob/ob mice highlight the complexity of the ghrelin-signaling pathway.

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Functional abnormalities of islets of Langerhans of obese hyperglycemic mouse.

Cited by 20 publications

References 6 publications

Increased concentration of fructose 2,6‐bisphosphate in livers of genetically obese mice

Increased concentration of fructose 2,6‐bisphosphate in livers of genetically obese mice

Differential control of muscle mass in type 1 and type 2 diabetes mellitus

Ablation of ghrelin receptor in leptin-deficient ob/ob mice has paradoxical effects on glucose homeostasis when compared with ablation of ghrelin in ob/ob mice

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