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Age and body weight effects on glucose and insulin tolerance in colony cats maintained since weaning on high dietary carbohydrate
Author(s) -
Backus R. C.,
Cave N. J.,
Ganjam V. K.,
Turner J. B. M.,
Biourge V. C.
Publication year - 2010
Publication title -
journal of animal physiology and animal nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.651
H-Index - 56
eISSN - 1439-0396
pISSN - 0931-2439
DOI - 10.1111/j.1439-0396.2010.01014.x
Subject(s) - medicine , insulin , endocrinology , insulin resistance , cats , diabetes mellitus , weaning , carbohydrate , pancreatic hormone , bolus (digestion) , biology
Summary High dietary carbohydrate is suggested to promote development of diabetes mellitus in cats. Glucose tolerance, insulin sensitivity, and insulin secretion were assessed in young [0.8–2.3 (median = 1.1) years, n  = 13] and mature [4.0–7.0 (median 5.8) years, n  = 12] sexually intact females of a large ( n  ≅ 700) feline colony in which only dry‐type diets (35% metabolizable energy as carbohydrate) were fed from weaning. Insulin sensitivity was assessed from the ‘late‐phase’ (60–120 min) plasma insulin response of intravenous glucose tolerance tests (IVGTTs) and from fractional change in glycaemia from baseline 15 min after an insulin bolus (0.1 U/kg, i.v.). Insulin secretion was assessed from the ‘early‐phase’ (0–15 min) plasma insulin response of IVGTTs. Compared to the young cats, the mature cats had greater body weights [2.3–3.8 (median = 2.9) vs. 3.0–6.3 (median = 4.0) kg, p < 0.01], greater late‐phase insulin responses (p < 0.05), lower insulin‐induced glycaemic changes (p = 0.06), lower early‐phase insulin responses (p < 0.05), and non‐significantly different rates of glucose disposal. The late‐phase insulin response was correlated with body weight and age (p < 0.05). When group assignments were balanced for body weight, the age‐group differences and correlations became non‐significant. The findings indicate that body weight gain is more likely than dry‐type diets to induce the pre‐diabetic conditions of insulin resistance and secretion dysfunction.

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