Metabolism of Glucose in the Small Intestine of Lean and Obese (ob/ob) Mice

Hanson, Peter J.; Morton, Ann P.

doi:10.1159/000176711

Cited by 6 publications

(3 citation statements)

References 15 publications

(12 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As the slope of the increase in EE in the Scholander experiments was not different between WT and ob/ob mice, a defect in insulation was not driving increases in EE. The mice did not show significant differences in food intake, as compared to WT controls (Figure S2J), which is most likely a reflection of their age; ob/ob mice show only a transient hyperphagic phase (Figure S1A) (Hanson and Morton, 1983). Thus, the explanation for the higher EE of the ob/ob mice cannot be a higher thermic effect of food as a result of hyperphagia.…”

Section: Ob/ob Mice Are Not Hypometabolicmentioning

confidence: 90%

Leptin Raises Defended Body Temperature without Activating Thermogenesis

et al. 2016

View full text Add to dashboard Cite

Leptin has been believed to exert its weight-reducing action not only by inducing hypophagia but also by increasing energy expenditure/thermogenesis. Leptin-deficient ob/ob mice have correspondingly been thought to be thermogenically limited and to show hypothermia, mainly due to atrophied brown adipose tissue (BAT). In contrast to these established views, we found that BAT is fully functional and that leptin treatment did not increase thermogenesis in wild-type or in ob/ob mice. Rather, ob/ob mice showed a decreased but defended body temperature (i.e., were anapyrexic, not hypothermic) that was normalized to wild-type levels after leptin treatment. This was not accompanied by increased energy expenditure or BAT recruitment but, instead, was mediated by decreased tail heat loss. The weight-reducing hypophagic effects of leptin are, therefore, not augmented through a thermogenic effect of leptin; leptin is, however, pyrexic, i.e., it alters centrally regulated thresholds of thermoregulatory mechanisms, in parallel to effects of other cytokines.

show abstract

Section: Ob/ob Mice Are Not Hypometabolicmentioning

confidence: 90%

Leptin Raises Defended Body Temperature without Activating Thermogenesis

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Five to 10-week-old ob/ob mice are hyperphagic, obese, and hyperinsulinemic and exhibit hypertrophy and length increase of small intestine which persist in 20-week-old mice [90,146,272]. Absorption of 10 mM and 28 mM D-glucose per unit small intestinal length in 10 and 20-week-old ob/ob mice was higher compared to lean wild-type mice, whereas Dglucose absorption related to small intestinal weight was not different [272].…”

Section: Rodent Models Of Type 2 Diabetesmentioning

confidence: 94%

Glucose transporters in the small intestine in health and disease

Koepsell

2020

Pflugers Arch - Eur J Physiol

173

146

View full text Add to dashboard Cite

Absorption of monosaccharides is mainly mediated by Na +-D-glucose cotransporter SGLT1 and the facititative transporters GLUT2 and GLUT5. SGLT1 and GLUT2 are relevant for absorption of D-glucose and D-galactose while GLUT5 is relevant for D-fructose absorption. SGLT1 and GLUT5 are constantly localized in the brush border membrane (BBM) of enterocytes, whereas GLUT2 is localized in the basolateral membrane (BLM) or the BBM plus BLM at low and high luminal D-glucose concentrations, respectively. At high luminal D-glucose, the abundance SGLT1 in the BBM is increased. Hence, D-glucose absorption at low luminal glucose is mediated via SGLT1 in the BBM and GLUT2 in the BLM whereas high-capacity D-glucose absorption at high luminal glucose is mediated by SGLT1 plus GLUT2 in the BBM and GLUT2 in the BLM. The review describes functions and regulations of SGLT1, GLUT2, and GLUT5 in the small intestine including diurnal variations and carbohydrate-dependent regulations. Also, the roles of SGLT1 and GLUT2 for secretion of enterohormones are discussed. Furthermore, diseases are described that are caused by malfunctions of small intestinal monosaccharide transporters, such as glucose-galactose malabsorption, Fanconi syndrome, and fructose intolerance. Moreover, it is reported how diabetes, small intestinal inflammation, parental nutrition, bariatric surgery, and metformin treatment affect expression of monosaccharide transporters in the small intestine. Finally, food components that decrease D-glucose absorption and drugs in development that inhibit or downregulate SGLT1 in the small intestine are compiled. Models for regulations and combined functions of glucose transporters, and for interplay between D-fructose transport and metabolism, are discussed.

show abstract

“…Obese mouse models also show an increase in intestinal absorption 6 and permeability 7 . It appears that the intestinal adaptation in the these animals may be due to the hyperphagia that occurs in all models (VMH lesions 6,8 , ob/ob 6,9 and db/db 10 mice, goldthioglucose 6 ). Since Mayer and Yannoni 6 had postulated that it is the hyperphagia that occurs with obesity, regardless of the etiology, that results in adaptive changes in the intestine, it has become well established that luminal nutrients are necessary for the growth of the mucosal epithelium.…”

Section: Introductionmentioning

confidence: 97%

Nutrient-induced intestinal adaption and its effect in obesity

Dailey

2014

Physiology & Behavior

View full text Add to dashboard Cite

Obese and lean individuals respond differently to nutrients with changes in digestion, absorption and hormone release. This may be a result of differences in intestinal epithelial morphology and function driven by the hyperphagia or the type of diet associated with obesity. It is well known that the maintenance and growth of the intestine is driven by the amount of luminal nutrients, with high nutrient content resulting in increases in cell number, villi length and crypt depth. In addition, the type of nutrient appears to contribute to alterations in the morphology and function of the epithelial cells. This intestinal adaptation may be what is driving the differences in nutrient processing in lean versus obese individuals. This review describes how nutrients may be able to induce changes in intestinal epithelial cell proliferation, differentiation and function and the link between intestinal adaptation and obesity.

show abstract

Metabolism of Glucose in the Small Intestine of Lean and Obese (ob/ob) Mice

Cited by 6 publications

References 15 publications

Leptin Raises Defended Body Temperature without Activating Thermogenesis

Leptin Raises Defended Body Temperature without Activating Thermogenesis

Glucose transporters in the small intestine in health and disease

Nutrient-induced intestinal adaption and its effect in obesity

Contact Info

Product

Resources

About