Concomitant food intake and adipose tissue responses under chronic insulin infusion in rats

Larue-Achagiotis, Christiane; Goubern, Marc; Laury, M C

doi:10.1016/0031-9384(88)90351-4

Cited by 12 publications

(6 citation statements)

References 23 publications

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“…Additionally, they investigated the satiety-reducing effect of insulin detemir, and found lower expression of two hypothalamic appetite-regulating neuropeptides, neuropeptide Y and galanin, with insulin detemir compared with insulin glargine (p < 0.05). In marked contrast to other studies in non-diabetic normal weight and overweight rats, which often show insulin-induced hyperphagia and weight gain [21][22][23], these investigations show that insulin detemir is associated with decreased cumulative food intake and less weight gain in rats even in the absence of hypoglycaemia, and further indicate that inhibitory effects of insulin detemir on appetite are increased in the context of high-fat diets or obesity. Clinical studies have corroborated the negative correlation between weight gain and body mass index (BMI) with insulin detemir treatment, i.e.…”

Section: Animal Studiescontrasting

confidence: 99%

Weight‐sparing effect of insulin detemir: a consequence of central nervous system‐mediated reduced energy intake?

Russell‐Jones

Danne

Hermansen

et al. 2015

Diabetes Obesity Metabolism

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Insulin therapy is often associated with adverse weight gain. This is attributable, at least in part, to changes in energy balance and insulin's anabolic effects. Adverse weight gain increases the risk of poor macrovascular outcomes in people with diabetes and should therefore be mitigated if possible. Clinical studies have shown that insulin detemir, a basal insulin analogue, exerts a unique weight‐sparing effect compared with other basal insulins. To understand this property, several hypotheses have been proposed. These explore the interplay of efferent and afferent signals between the muscles, brain, liver, renal and adipose tissues in response to insulin detemir and comparator basal insulins. The following models have been proposed: insulin detemir may reduce food intake through direct or indirect effects on the central nervous system (CNS); it may have favourable actions on hepatic glucose metabolism through a selective effect on the liver, or it may influence fluid homeostasis through renal effects. Studies have consistently shown that insulin detemir reduces energy intake, and moreover, it is clear that this shift in energy balance is not a consequence of reduced hypoglycaemia. CNS effects may be mediated by direct action, by indirect stimulation by peripheral mediators and/or via a more physiological counter‐regulatory response to insulin through restoration of the hepatic–peripheral insulin gradient. Although the precise mechanism remains unclear, it is likely that the weight‐sparing effect of insulin detemir can be explained by a combination of mechanisms. The evidence for each hypothesis is considered in this review.

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Section: Animal Studiescontrasting

confidence: 99%

Weight‐sparing effect of insulin detemir: a consequence of central nervous system‐mediated reduced energy intake?

Russell‐Jones

Danne

Hermansen

et al. 2015

Diabetes Obesity Metabolism

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“…More details in Fig. 1 expected, in view of the anabolic action of insulin in fish [30] and the insulin-induced lipogenesis in hyperinsulinemic rats [53,54]. However, the global inhibition of ACLY by insulin is surprising although consistent, since it was found at all the levels studied.…”

Section: Lipogenesis In White Adipose Tissuementioning

confidence: 62%

Insulin Stimulates Lipogenesis and Attenuates Beta‐Oxidation in White Adipose Tissue of Fed Rainbow Trout

Polakof

Médale

Larroquet

et al. 2011

Lipids

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As lipid deposition tissue in fish, the white adipose tissue (WAT) has important functions related to reproduction and the challenges of long-term fasting. In the study reported here, we infused fish fed a high-carbohydrate diet with two doses of insulin for 5 days in order to explore the effects of this hormone on lipogenesis and beta-oxidation-related enzymes. We demonstrated the presence of some of the main lipogenic enzymes at molecular, protein and activity levels (ATP-citrate lyase and fatty acid synthase). However, while ATP-citrate lyase was unexpectedly down-regulated, fatty acid synthase was up-regulated (at protein and activity levels) in an insulin dose-dependent manner. The main enzymes acting as NADPH donors for lipogenesis were also characterized at biochemical and molecular levels, although there was no evidence of their regulation by insulin. On the other hand, lipid oxidation potential was found in this tissue through the measurement of gene expression of enzymes involved in β-oxidation, highlighting two carnitine palmitoyltransferase isoforms, both down-regulated by insulin infusion. We found that insulin acts as an important regulator of trout WAT lipid metabolism, inducing the final stage of lipogenesis at molecular, protein and enzyme activity levels and suppressing β-oxidation at least at a molecular level. These results suggest that WAT in fish may have a role that is important not only as a lipid deposition tissue but also as a lipogenic organ (with possible involvement in glucose homeostasis) that could also be able to utilize the lipids stored as a local energy source.

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“…39, 40, 41, 42, 43, 44, 45 Notably, only a study by Vanderweele 46 showed an 11% reduction of spontaneous daily food intake in normal-weight chow-fed rats administered 2 U per day of regular insulin via an osmotic minipump implanted into the peritoneal cavity. Thus, our findings with insulin Det appear to be fundamentally novel.…”

Section: Discussionmentioning

confidence: 99%

Insulin detemir attenuates food intake, body weight gain and fat mass gain in diet-induced obese Sprague–Dawley rats

2011

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Objective:Initiation and intensification of insulin therapy commonly causes weight gain, a barrier to therapy. A contrasting body of evidence indicates that insulin functions as an adiposity negative feedback signal and reduces food intake, weight gain and adiposity via action in the central nervous system. Basal insulin analogs, detemir (Det) and glargine (Glar), have been associated with less hypoglycemia compared with neutral protamine hagedorn insulin, and Det with less weight gain, especially in patients with higher body mass index (BMI). We sought to determine whether insulin therapy per se causes body weight and fat mass gain when delivered via a clinically relevant subcutaneous (SC) route in the absence of hypoglycemia and glycosuria in non-diabetic lean and diet-induced obese rats.Materials and methods:Rats were exposed to either a low-fat diet (LFD; 13.5% fat) or high-fat diet (HFD; 60% fat), and received Det (0.5 U kg−1), Glar (0.2 U kg−1) or vehicle (Veh) SC once daily for 4 weeks. These dosages of insulin were equipotent in rats with respect to blood–glucose concentration and did not induce hypoglycemia.Results:As predicted by current models of energy homeostasis, neither insulin Det nor Glar therapy affected food intake and weight gain in LFD rats. Det treatment significantly attenuated food intake, body weight gain and fat mass gain relative to the Glar and Veh in high-fat fed animals, mirroring observations in humans.Conclusions:That neither insulin group gained excess weight, suggests weight gain with SC basal insulin therapy may not be inevitable. Our data further suggest that Det possesses a unique property to attenuate the development of obesity associated with a HFD.

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Concomitant food intake and adipose tissue responses under chronic insulin infusion in rats

Cited by 12 publications

References 23 publications

Weight‐sparing effect of insulin detemir: a consequence of central nervous system‐mediated reduced energy intake?

Weight‐sparing effect of insulin detemir: a consequence of central nervous system‐mediated reduced energy intake?

Insulin Stimulates Lipogenesis and Attenuates Beta‐Oxidation in White Adipose Tissue of Fed Rainbow Trout

Insulin detemir attenuates food intake, body weight gain and fat mass gain in diet-induced obese Sprague–Dawley rats

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