The monocarboxylate transporter 1 (MCT1 or SLC16A1) is a carrier of short-chain fatty acids, ketone bodies, and lactate in several tissues. Genetically modified C57BL/6J mice were produced by targeted disruption of the mct1 gene in order to understand the role of this transporter in energy homeostasis. Null mutation was embryonically lethal, but MCT1+/− mice developed normally. However, when fed high fat diet (HFD), MCT1+/− mice displayed resistance to development of diet-induced obesity (24.8% lower body weight after 16 weeks of HFD), as well as less insulin resistance and no hepatic steatosis as compared to littermate MCT1+/+ mice used as controls. Body composition analysis revealed that reduced weight gain in MCT1+/− mice was due to decreased fat accumulation (50.0% less after 9 months of HFD) notably in liver and white adipose tissue. This phenotype was associated with reduced food intake under HFD (12.3% less over 10 weeks) and decreased intestinal energy absorption (9.6% higher stool energy content). Indirect calorimetry measurements showed ∼ 15% increase in O2 consumption and CO2 production during the resting phase, without any changes in physical activity. Determination of plasma concentrations for various metabolites and hormones did not reveal significant changes in lactate and ketone bodies levels between the two genotypes, but both insulin and leptin levels, which were elevated in MCT1+/+ mice when fed HFD, were reduced in MCT1+/− mice under HFD. Interestingly, the enhancement in expression of several genes involved in lipid metabolism in the liver of MCT1+/+ mice under high fat diet was prevented in the liver of MCT1+/− mice under the same diet, thus likely contributing to the observed phenotype. These findings uncover the critical role of MCT1 in the regulation of energy balance when animals are exposed to an obesogenic diet.

https://serval.unil.ch/resource/serval:BIB_7C2648899BDB.P001/REF.pdf

Resistance to Diet-Induced Obesity and Associated Metabolic Perturbations in Haploinsufficient Monocarboxylate Transporter 1 Mice

Doves, Diplomats, and Diabetes

Readers are bound to wonder why in a book on diabetes we have not discussed blood sugar levels at sufficient length so far and why it is delayed till the 12th chapter. The common perception of diabetes begins with blood sugar and often ends with blood sugar. We saw in Chap. 3 that there are a series of paradoxes associated with the existing theory of glucose homeostasis and the conventionally perceived etiology of hyperglycemia. The alternative picture needs to resolve all the paradoxes. We can attempt to do so at this stage since by now I think sufficient background about the new interpretation has been built on which we can construct a new model of normal glucose regulation and altered glucose dynamics in T2D. Discussing sugar so late in this book also serves as a gesture intended to emphasize that sugar levels in blood are actually not as important in diabetes as generally believed. Raised blood sugar to diabetes is just what fever is to typhoid. It is only one of the many symptoms. However, it is one that is easiest to monitor and therefore the first indication in diagnosis and one that can also be conveniently used to follow the progression of the illness as well as any recovery from it. But that is its limitation. Just as fever is not everything in typhoid, blood sugar is not everything in T2D. Typhoid is an infection, and fever is only a symptom. If typhoid is cured, fever will certainly vanish, and the body temperature will return to normal. The reverse is not true. Fever can be reduced by antipyretic drugs or other physical means. Keeping the body on ice can also reduce the body temperature temporarily. But fever gone is not typhoid gone. The relation of blood sugar to T2D is very similar. Bringing blood sugar back to normal is not an indication of diabetes gone.

Why Blood Sugar Goes Up

Orlistat-induced weight loss results in amelioration in several comorbidities including obesity-related dyslipidemia. The aim of the present study was to characterize the changes in the blood plasma metabolic profile from overweight women treated with Orlistat, a lipase inhibitor. A metabonomic approach employing HNMR was applied to the access metabolic profile in lean and overweight women after a 120 day treatment with 120 mg of Orlistat three times daily. Twenty overweight women (BMI: 32.8 ± 2.9 kg/m) were evaluated before and after Orlistat treatment and seven normal weight women (BMI: 21.8 ± 1.4 kg/m) were taken as control. After 120 days of treatment with Orlistat, no significant weight changes were observed. However, Orlistat-induced metabolic changes in overweight subjects decreased the profile differences between lean and obese individuals, independent of weight loss. These were associated to decreasing levels of lactate and calcium. Higher levels of lactate, alanine and lipids from overweight subjects were detected in comparison to lean individuals. These results show that a lipase inhibitor shifts the metabolic profile of overweight subjects towards normality, independent of weight loss.

Orlistat-lnduced Modulation of Plasma Metabolites Independent of Weight Loss in Overweight Females

Orlistat-Induced Modulation of Plasma Metabolites Independent of Weight Loss in Overweight Females

Low plasma lactate concentration as a biomarker of an incompetent brain-pull: A risk factor for weight gain in type 2 diabetes patients

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Low plasma lactate concentration as a biomarker of an incompetent brain-pull: A risk factor for weight gain in type 2 diabetes patients