Increased islet volume but unchanged islet number in ob/ob mice.
نویسندگان
چکیده
It is important for our understanding of the pancreatic islets to study whether new islets are able to form in the intact pancreas. We developed a new method to determine the total number and the mean volume of the pancreatic islets, and we used this method to study the expansion of the islet mass in ob/ob mice (n = 8), using ob/+ mice (n = 8) as controls. The total islet volume was increased by a factor of 3.6 in ob/ob mice compared with ob/+ mice, whereas, importantly, the total number of islets did not differ among ob/ob mice and ob/+ mice (3,193 +/- 160 islets in ob/ob mice vs. 3,184 +/- 142 islets in ob/+ mice, P = 0.97). The coefficient of variation in the volume distribution of islets was equal in the two groups, showing that in ob/ob mice, the existing islets expand their volume by the same proportion, without a net formation of new islets. We suggest that the pancreatic islets should be considered as anatomically such complex structures that islet neogenesis does not spontaneously occur in an intact pancreas. Cells within the existing islets are presumably the most important sources for islet cell hyperplasia during expansion of the total islet mass.
منابع مشابه
Pancreatic Islet Vasculature Adapts to Insulin Resistance Through Dilation and Not Angiogenesis
Pancreatic islets adapt to insulin resistance through a complex set of changes, including β-cell hyperplasia and hypertrophy. To determine if islet vascularization changes in response to insulin resistance, we investigated three independent models of insulin resistance: ob/ob, GLUT4(+/-), and mice with high-fat diet-induced obesity. Intravital blood vessel labeling and immunocytochemistry revea...
متن کاملIntra-islet lesions and lobular variations in β-cell mass expansion in ob/ob mice revealed by 3D imaging of intact pancreas
The leptin deficient ob/ob mouse is a widely used model for studies on initial aspects of metabolic disturbances leading to type 2 diabetes, including insulin resistance and obesity. Although it is generally accepted that ob/ob mice display a dramatic increase in β-cell mass to compensate for increased insulin demand, the spatial and quantitative dynamics of β-cell mass distribution in this mod...
متن کاملIslet cell surface antibodies in genetically obese hyperglycaemic (ob/ob) mice.
A quantitative method for circulating islet cell surface antibodies (ICSA), based on the binding of 125I-protein A to insulin-producing RINm5F cells, was used to evaluate ICSA in plasma of 4- to 40-week-old Aston obese hyperglycaemic (ob/ob) mice and normal control (+/+) mice. RINm5F cells bound 2502 +/- 1196 c.p.m. 125I-protein A per 10(5) cells (mean +/- S.D., n = 54) after incubation with +/...
متن کاملNon-Invasive Bioluminescence Imaging of β-Cell Function in Obese-Hyperglycemic [ob/ob] Mice
BACKGROUND Type 2 diabetes results from failure of the β-cells to compensate for increased insulin demand due to abnormal levels of metabolic factors. The ob/ob(lep-/-) mouse has been extensively studied as an animal model of type 2 diabetes. Previous studies have shown a correlation between β-cell function and bioluminescent imaging in lean genetically engineered mice. The ability to noninvasi...
متن کاملElimination of glucagon-like peptide 1R signaling does not modify weight gain and islet adaptation in mice with combined disruption of leptin and GLP-1 action.
Leptin and glucagon-like peptide 1 (GLP-1) exhibit opposing actions in the endocrine pancreas. GLP-1 stimulates insulin biosynthesis, secretion, and islet growth, whereas leptin inhibits glucose-dependent insulin secretion and insulin gene transcription. In contrast, GLP-1 and leptin actions overlap in the central nervous system, where leptin has been shown to activate GLP-1 circuits that inhib...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Diabetes
دوره 52 7 شماره
صفحات -
تاریخ انتشار 2003