Glycogen and adipose tissue

Tuerkischer, E.; Wertheimer, Ernst

doi:10.1113/jphysiol.1942.sp003950

Cited by 148 publications

(36 citation statements)

References 6 publications

(7 reference statements)

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“…This conclusion is consistent with previous findings showing that adipose triglyceride stores are primarily synthesized within adipose tissue, rather than being imported into fat (22). Adipose tissue from animals re-fed after a 48 h fast was previously shown to have a respiratory quotient of Ͼ1.0, indicative of a high rate of glucose metabolism and not fatty acids (23,25). In re-fed animals, glycogen disappears from adipose tissue at the same time as fatty acid synthesis is maximal, and PAS-positive material and lipid droplets can be easily seen in the same cells during the recovery from weight loss (see Fig.…”

Section: Discussionsupporting

confidence: 91%

“…The initial phase of this cellular program is marked by an increase in adipocyte glycogen content. The glycogen content of white adipose tissue is normally exceedingly low (20) and previous studies have shown that fasting reduces glycogen levels even further, while subsequent refeeding transiently increases adipose tissue glycogen content (21)(22)(23). Because glycogen content increases after leptin withdrawal, even in the absence of hyperinsulinemia, we conclude that the observed increase in glycogen synthesis in white adipose tissue after refeeding is induced by low leptin levels (24).…”

Section: Discussionsupporting

confidence: 54%

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Cellular program controlling the recovery of adipose tissue mass: An in vivo imaging approach

Birsoy

Soukas²,

Torréns³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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The cellular program responsible for the restoration of adipose tissue mass after weight loss is largely uncharacterized. Leptin mRNA levels are highly correlated with adipose tissue mass, and leptin expression can thus be used as a surrogate for changes in the amount of adipose tissue. To further study the responses of adipocytes to changes in weight, we created a transgenic mouse expressing the luciferase reporter gene under the control of leptin regulatory sequences, which allows noninvasive imaging of the leptin expression of mice in vivo. We used these animals to show that weight loss induced by fasting or leptin treatment results in the retention of lipid-depleted adipocytes in adipose depots. To further study the cellular response to weight regain after leptin treatment, a leptin withdrawal protocol was used to induce a state of acute leptin deficiency in wild type mice. Acute leptin deficiency led to the transient deposition of large amounts of glycogen within pre-existing, lipid-depleted adipocytes. This was followed by rapid reaccumulation of lipid. Transcriptional profiling revealed that this cellular response was associated with induction of mRNAs for the entire pathway of enzymes necessary to convert glucose into acetyl-CoA and glycerol, key substrates for the synthesis of triglycerides.adipocytes ͉ leptin ͉ luciferase

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 54%

Cellular program controlling the recovery of adipose tissue mass: An in vivo imaging approach

Birsoy

Soukas²,

Torréns³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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“…Thus, only under specific challenging situations (other than diet-induced obesity) might the inability of beta cells to synthesise glycogen have a measurable impact on beta cell function and whole-body glucose homeostasis. For instance, tissue-specific functions of glycogen have been observed in adipocytes, where it provides glycerol for triacylglycerol synthesis in the fasting to feeding transition [36] and modulates lipid metabolism after a switch from a high-fat to a standard chow diet [37]. Likewise, in neurons, glycogen has been shown to contribute to tolerance to hypoxia [38].…”

Section: Discussionmentioning

confidence: 99%

Genetic models rule out a major role of beta cell glycogen in the control of glucose homeostasis

et al. 2016

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Aims/hypothesis Glycogen accumulation occurs in beta cells of diabetic patients and has been proposed to partly mediate glucotoxicity-induced beta cell dysfunction. However, the role of glycogen metabolism in beta cell function and its contribution to diabetes pathophysiology remain poorly understood. We investigated the function of beta cell glycogen by studying glucose homeostasis in mice with (1) defective glycogen synthesis in the pancreas; and (2) excessive glycogen accumulation in beta cells. Methods Conditional deletion of the Gys1 gene and overexpression of protein targeting to glycogen (PTG) was accomplished by Cre-lox recombination using pancreasspecific Cre lines. Glucose homeostasis was assessed by determining fasting glycaemia, insulinaemia and glucose tolerance. Beta cell mass was determined by morphometry. Glycogen was detected histologically by periodic acidSchiff's reagent staining. Isolated islets were used for the determination of glycogen and insulin content, insulin secretion, immunoblots and gene expression assays. Results Gys1 knockout (Gys1 KO ) mice did not exhibit differences in glucose tolerance or basal glycaemia and insulinaemia relative to controls. Insulin secretion and gene expression in isolated islets was also indistinguishable between Gys1 KO and controls. Conversely, despite effective glycogen overaccumulation in islets, mice with PTG overexpression (PTG OE ) presented similar glucose tolerance to controls. However, under fasting conditions they exhibited lower glycaemia and higher insulinaemia. Importantly, neither young nor aged PTG OE mice showed differences in beta cell mass relative to age-matched controls. Finally, a high-fat diet did not reveal a beta cell-autonomous phenotype in either model. Conclusions/interpretation Glycogen metabolism is not required for the maintenance of beta cell function. Glycogen accumulation in beta cells alone is not sufficient to trigger the dysfunction or loss of these cells, or progression to diabetes.

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“…Insulin is required for glycogen deposition in adipose tissue (Tuerkischer & Wertheimer, 1942, 1946Engel, 1951) and is opposed in its action by cortisol (Lundquist, 1968;Leboeuf, Renold & Cahill, 1962). The high concentration of glycogen in the perirenal fat and its apparent depletion after cortisol infusion in adrenalectomized and hypophysectomized foetuses suggests a possible insulin dominance of carbohydrate metabolism in these animals.…”

Section: Discussionmentioning

confidence: 99%

Effect of cortisol on liver glycogen concentrations in hypophysectomized, adrenalectomized and normal foetal lambs during late or prolonged gestation.

Barnes¹,

Comline²,

Silver³

1978

The Journal of Physiology

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SUMMARY1. The changes in liver glycogen concentration in normal, adrenalectomized and hypophysectomized foetal lambs have been examined during the last third of gestation using a biopsy technique to remove one or more samples of liver from the same foetus at different gestational ages.2. The rate of glycogen deposition increased sharply from about 130 days' gestation in normal lamb foetuses whereas after hypophysectomy or adrenalectomy liver glycogen concentrations remained low even when gestation was prolonged.3. i.v. infusions of cortisol (4-10 mg/day) for 52 hr resulted in four-to fivefold increases in liver glycogen in all three groups of foetuses. The level of glycogen in the liver appeared to be related to log plasma corticosteroid concentration in all foetuses whether they had received cortisol infusions or not.4. Little or no change occurred in glycogen concentration in other foetal tissues apart from a decrease in the glycogen levels in peri-renal fat of adrenalectomized and hypophysectomized foetuses after cortisol infusion. There were also no detectable changes in foetal plasma lactate, urea or a amino nitrogen following the cortisol infusions. Foetal plasma glucose values rose slightly but this change was significant only in the adrenalectomized group.5. The 52 hr cortisol infusions to the foetus resulted in a slight but significant fall in maternal plasma progesterone in the last few hours of the infusion period.

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Glycogen and adipose tissue

Cited by 148 publications

References 6 publications

Cellular program controlling the recovery of adipose tissue mass: An in vivo imaging approach

Cellular program controlling the recovery of adipose tissue mass: An in vivo imaging approach

Genetic models rule out a major role of beta cell glycogen in the control of glucose homeostasis

Effect of cortisol on liver glycogen concentrations in hypophysectomized, adrenalectomized and normal foetal lambs during late or prolonged gestation.

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